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Correlation between Nutrition, Oxidative Stress and Disease 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 25958

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Guest Editor

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Guest Editor
Department of Medicine and Science of Aging, University “G. D’Annunzio”, 66100 Chieti, Italy
Interests: nutrition; oxidative stress; cellular biology; disease; antioxidant; bioactive vegetable; molecules; endogenous antioxidant enzymes; vegetable food; nitric oxide; inflammation diseases, inflammatory bowel disease
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Special Issue Information

Dear Colleagues, 

When the regulation of radical homeostasis in tissues or cells does not function correctly, a situation of stress can come about, due to the increased presence of oxidative radicals. In these cases, the term “oxidative stress” is often used to indicate an imbalance towards major tissue oxidation, measured by the appearance of oxidized species, including lipids, proteins, DNA, and carbohydrates. A strong relationship exists between nutrition and oxidative stress. Works that have been published in recent years in the field of human health, demonstrate that the production, transformation, and metabolism of free radicals are finely regulated processes, and that their malfunction inevitably leads to inflammatory tissue damage. On the other hand, oxidative stress has to be considered not only as a negative event but also as a physiological process. For example, a transient situation of oxidative stress constitutes one of the fundamental functional mechanisms of many chemical mediators (hormones, neurotransmitters, cytokines, etc.), in the defense from infective agents, and for the alteration of the redox state, which is necessary to start differentiation processes. On the other hand, the chronicity of oxidative stress constitutes a condition of risk for degenerative processes and can lead to a pathological situation. A varied, balanced, and good-quality diet can supply a majority of antioxidant substances that can act in synergy to obstruct the excessive presence of free radicals. In addition, it is essential that a diet be rich in foods of vegetable origin, which are the true allies in tackling the damages associated with an alteration of the redox cellular state.

Prof. Dr. Sara Franceschelli
Prof. Dr. Lorenza Speranza
Guest Editors

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Keywords

  • nutrition
  • oxidative stress 
  • disease 
  • antioxidant 
  • bioactive vegetable molecules 
  • superoxide dismutase 
  • catalase 
  • vegetable food 
  • polyphenol 
  • α-mangostin

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22 pages, 3905 KiB  
Article
Specific Post-Translational Modifications of VDAC3 in ALS-SOD1 Model Cells Identified by High-Resolution Mass Spectrometry
by Maria Gaetana Giovanna Pittalà, Simona Reina, Stefano Conti Nibali, Annamaria Cucina, Salvatore Antonio Maria Cubisino, Vincenzo Cunsolo, Giuseppe Federico Amodeo, Salvatore Foti, Vito De Pinto, Rosaria Saletti and Angela Messina
Int. J. Mol. Sci. 2022, 23(24), 15853; https://doi.org/10.3390/ijms232415853 - 13 Dec 2022
Cited by 6 | Viewed by 1949
Abstract
Damage induced by oxidative stress is a key driver of the selective motor neuron death in amyotrophic lateral sclerosis (ALS). Mitochondria are among the main producers of ROS, but they also suffer particularly from their harmful effects. Voltage-dependent anion-selective channels (VDACs) are the [...] Read more.
Damage induced by oxidative stress is a key driver of the selective motor neuron death in amyotrophic lateral sclerosis (ALS). Mitochondria are among the main producers of ROS, but they also suffer particularly from their harmful effects. Voltage-dependent anion-selective channels (VDACs) are the most represented proteins of the outer mitochondrial membrane where they form pores controlling the permeation of metabolites responsible for mitochondrial functions. For these reasons, VDACs contribute to mitochondrial quality control and the entire energy metabolism of the cell. In this work we assessed in an ALS cell model whether disease-related oxidative stress induces post-translational modifications (PTMs) in VDAC3, a member of the VDAC family of outer mitochondrial membrane channel proteins, known for its role in redox signaling. At this end, protein samples enriched in VDACs were prepared from mitochondria of an ALS model cell line, NSC34 expressing human SOD1G93A, and analyzed by nUHPLC/High-Resolution nESI-MS/MS. Specific over-oxidation, deamidation, succination events were found in VDAC3 from ALS-related NSC34-SOD1G93A but not in non-ALS cell lines. Additionally, we report evidence that some PTMs may affect VDAC3 functionality. In particular, deamidation of Asn215 alone alters single channel behavior in artificial membranes. Overall, our results suggest modifications of VDAC3 that can impact its protective role against ROS, which is particularly important in the ALS context. Data are available via ProteomeXchange with identifier PXD036728. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 3.0)
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19 pages, 3296 KiB  
Article
Unique Role of Caffeine Compared to Other Methylxanthines (Theobromine, Theophylline, Pentoxifylline, Propentofylline) in Regulation of AD Relevant Genes in Neuroblastoma SH-SY5Y Wild Type Cells
by Daniel Janitschke, Anna A. Lauer, Cornel M. Bachmann, Martin Seyfried, Heike S. Grimm, Tobias Hartmann and Marcus O. W. Grimm
Int. J. Mol. Sci. 2020, 21(23), 9015; https://doi.org/10.3390/ijms21239015 - 27 Nov 2020
Cited by 12 | Viewed by 3608
Abstract
Methylxanthines are a group of substances derived from the purine base xanthine with a methyl group at the nitrogen on position 3 and different residues at the nitrogen on position 1 and 7. They are widely consumed in nutrition and used as pharmaceuticals. [...] Read more.
Methylxanthines are a group of substances derived from the purine base xanthine with a methyl group at the nitrogen on position 3 and different residues at the nitrogen on position 1 and 7. They are widely consumed in nutrition and used as pharmaceuticals. Here we investigate the transcriptional regulation of 83 genes linked to Alzheimer’s disease in the presence of five methylxanthines, including the most prominent naturally occurring methylxanthines—caffeine, theophylline and theobromine—and the synthetic methylxanthines pentoxifylline and propentofylline. Methylxanthine-regulated genes were found in pathways involved in processes including oxidative stress, lipid homeostasis, signal transduction, transcriptional regulation, as well as pathways involved in neuronal function. Interestingly, multivariate analysis revealed different or inverse effects on gene regulation for caffeine compared to the other methylxanthines, which was further substantiated by multiple comparison analysis, pointing out a distinct role for caffeine in gene regulation. Our results not only underline the beneficial effects of methylxanthines in the regulation of genes in neuroblastoma wild-type cells linked to neurodegenerative diseases in general, but also demonstrate that individual methylxanthines like caffeine mediate unique or inverse expression patterns. This suggests that the replacement of single methylxanthines by others could result in unexpected effects, which could not be anticipated by the comparison to other substances in this substance class. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 2.0)
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16 pages, 3498 KiB  
Article
Resveratrol, Curcumin and Piperine Alter Human Glyoxalase 1 in MCF-7 Breast Cancer Cells
by Betina Schmidt, Christian Ferreira, Carlos Luan Alves Passos, Jerson Lima Silva and Eliane Fialho
Int. J. Mol. Sci. 2020, 21(15), 5244; https://doi.org/10.3390/ijms21155244 - 24 Jul 2020
Cited by 28 | Viewed by 4376
Abstract
Breast cancer is the leading cause of cancer mortality in women worldwide. Conventional cancer treatment is costly and results in many side effects. Dietary bioactive compounds may be a potential source for breast cancer prevention and treatment. In this scenario, the aim of [...] Read more.
Breast cancer is the leading cause of cancer mortality in women worldwide. Conventional cancer treatment is costly and results in many side effects. Dietary bioactive compounds may be a potential source for breast cancer prevention and treatment. In this scenario, the aim of this study was to investigate the effects of the bioactive compounds resveratrol, curcumin and piperine (R-C-P) on MCF-7 breast cancer cells and to associate them to Glyoxalase 1 (GLO1) activity. The findings indicate that R-C-P exhibits cytotoxicity towards MCF-7 cells. R-C-P decreased mitochondrial membrane potential (ΔΨm) by 1.93-, 2.04- and 1.17-fold, respectively. Glutathione and N-acetylcysteine were able to reverse the cytotoxicity of the assessed bioactive compounds in MCF-7 cells. R-C-P reduced GLO1 activity by 1.36-, 1.92- and 1.31-fold, respectively. R-C-P in the presence of antimycin A led to 1.98-, 1.65- and 2.16-fold decreases in D-lactate levels after 2 h of treatment, respectively. Glyoxal and methylglyoxal presented cytotoxic effects on MCF-7 cells, with IC50 values of 2.8 and 2.7 mM and of 1.5 and 1.4 mM after 24 and 48 h of treatment, respectively. In conclusion, this study demonstrated that R-C-P results in cytotoxic effects in MCF-7 cells and that this outcome is associated with decreasing GLO1 activity and mitochondrial dysfunction. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 2.0)
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14 pages, 4835 KiB  
Article
Salvianolic Acid B Slows the Progression of Breast Cancer Cell Growth via Enhancement of Apoptosis and Reduction of Oxidative Stress, Inflammation, and Angiogenesis
by Mohamed A. Katary, Rafik Abdelsayed, Abdulmohsin Alhashim, Mohamed Abdelhasib and Ahmed A. Elmarakby
Int. J. Mol. Sci. 2019, 20(22), 5653; https://doi.org/10.3390/ijms20225653 - 12 Nov 2019
Cited by 49 | Viewed by 4018
Abstract
Breast cancer is the current leading cause of cancer death in females worldwide. Although current chemotherapeutic drugs effectively reduce the progression of breast cancer, most of these drugs have many unwanted side effects. Salvianolic acid B (Sal-B) is a bioactive compound isolated from [...] Read more.
Breast cancer is the current leading cause of cancer death in females worldwide. Although current chemotherapeutic drugs effectively reduce the progression of breast cancer, most of these drugs have many unwanted side effects. Salvianolic acid B (Sal-B) is a bioactive compound isolated from the root of Danshen Radix with potent antioxidant and anti-inflammatory properties. Since free radicals play a key role in the initiation and progression of tumor cells growth and enhance their metastatic potential, the current study was designed to investigate the antitumor activity of Sal-B and compare it with the antitumor activity of the traditional anticancer drug, cisplatin. In vitro, Sal-B decreased the human breast cancer adenocarcinoma (MCF-7) cells proliferation in a concentration and time dependent manner. In vivo and similar to cisplatin treatment, Sal-B significantly reduced tumor volume and increased the median survival when compared to tumor positive control mice group injected with Ehrlich solid carcinoma cell line (ESC). Sal-B decreased plasma level of malondialdehyde as a marker of oxidative stress and increased plasma level of reduced glutathione (GSH) as a marker of antioxidant defense when compared to control ESC injected mice. Either Sal-B or cisplatin treatment decreased tumor tissue levels of tumor necrosis factor (TNF-α), matrix metalloproteinase-8 (MMP-8), and Cyclin D1 in ESC treated mice. Contrary to cisplatin treatment, Sal-B did not decrease tumor tissue Ki-67 protein in ESC injected mice. Immunohistochemical analysis revealed that Sal-B or cisplatin treatment increased the expression of the apoptotic markers caspase-3 and P53. Although Sal-B or cisplatin significantly reduced the expression of the angiogenic factor vascular endothelial growth factor (VEGF) in ESC injected mice, only Sal-B reduced expression level of COX-2 in ESC injected mice. Our data suggest that Sal-B exhibits antitumor features against breast cancer cells possibly via enhancing apoptosis and reducing oxidative stress, inflammation, and angiogenesis. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 2.0)
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18 pages, 2427 KiB  
Article
Modulation of CAT-2B-Mediated l-Arginine Uptake and Nitric Oxide Biosynthesis in HCT116 Cell Line Through Biological Activity of 4′-Geranyloxyferulic Acid Extract from Quinoa Seeds
by Sara Franceschelli, Daniela Maria Pia Gatta, Mirko Pesce, Alessio Ferrone, José Luis Quiles, Salvatore Genovese, Francesco Epifano, Serena Fiorito, Vito Alessandro Taddeo, Antonia Patruno, Alfredo Grilli, Mario Felaco and Lorenza Speranza
Int. J. Mol. Sci. 2019, 20(13), 3262; https://doi.org/10.3390/ijms20133262 - 2 Jul 2019
Cited by 11 | Viewed by 3200
Abstract
Chenopodium quinoa Wild is a “pseudocereal” grain which attracts a lot of attention in the scientific community as it has a positive effect on health. Here, we investigate the presence of biologically active O-prenylated phenylpropanoids in the ethanol extract of commercially available quinoa [...] Read more.
Chenopodium quinoa Wild is a “pseudocereal” grain which attracts a lot of attention in the scientific community as it has a positive effect on health. Here, we investigate the presence of biologically active O-prenylated phenylpropanoids in the ethanol extract of commercially available quinoa seeds. We claim that 4′-Geranyloxyferulic acid (GOFA) was the only phytochemical product found that belongs to quinoa’s group secondary metabolites. We studied the changes in the oxidative and inflammatory status of the cellular environment in HCT 116 cell line processed with quinoa extract and its component GOFA; the implementation was done through the analysis of the antioxidant enzymes (SOD and CAT), the pro-inflammatory components (iNOS, IL-6 and TNF-α), and the products of intermediary metabolism (ONOO, O2). Moreover, the l-arginine uptake was proposed as a target of the tested compounds. We demonstrated that the GOFA, through a decrease of the CAT-2B expression, leads to a reduction of the l-arginine uptake, downregulating the harmful iNOS and restoring the altered redox state. These results propose a new molecular target involved in the reduction of the critical inflammatory process responsible for the cancer progression. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 2.0)
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3739 KiB  
Article
Effect of Angelica sinensis Root Extract on Cancer Prevention in Different Stages of an AOM/DSS Mouse Model
by Bochen Zhao, Qian Kang, Yu Peng, Yuanping Xie, Cheng Chen, Bingshao Li and Qing Wu
Int. J. Mol. Sci. 2017, 18(8), 1750; https://doi.org/10.3390/ijms18081750 - 11 Aug 2017
Cited by 19 | Viewed by 6337
Abstract
Angelica sinensis root (ASR) extract was obtained to investigate its effects on colorectal carcinogenesis in different stages of an Azoxymethane/Dextran sodium sulphate (AOM/DSS) model. In this study, we showed that ASR extract administration in the initial stage of the AOM/DSS model had cancer [...] Read more.
Angelica sinensis root (ASR) extract was obtained to investigate its effects on colorectal carcinogenesis in different stages of an Azoxymethane/Dextran sodium sulphate (AOM/DSS) model. In this study, we showed that ASR extract administration in the initial stage of the AOM/DSS model had cancer preventive effects with decreasing tumor incidence and a high-grade of intraepithelial neoplasia incidence. With respect to DNA damage, the amounts of 8-oxoguanine and γ-H2AX were suppressed in colon tissue. The balance of apoptosis and proliferation was approaching the normal state. In contrast, ASR extract administration in the promotion stage of the AOM/DSS model accelerated the progression of carcinogenesis. The maximum tumor size reached 49.85 ± 25.04 mm3. High-grade pathological changes were significantly increased. Decreased DNA damage and P53 level reflected the disrupted reactive oxygen species (ROS) concentration in colorectal tissue, which led to an imbalance of proliferative and apoptotic relationships. These findings suggested that the cancer-preventive effect of ASR extract may be stage-dependent in the process of carcinogenesis. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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6247 KiB  
Article
A Novel Therapeutic Approach in the Treatment of Pulmonary Arterial Hypertension: Allium ursinum Liophylisate Alleviates Symptoms Comparably to Sildenafil
by Mariann Bombicz, Daniel Priksz, Balazs Varga, Andrea Kurucz, Attila Kertész, Akos Takacs, Aniko Posa, Rita Kiss, Zoltan Szilvassy and Bela Juhasz
Int. J. Mol. Sci. 2017, 18(7), 1436; https://doi.org/10.3390/ijms18071436 - 4 Jul 2017
Cited by 16 | Viewed by 7055
Abstract
Right-sided heart failure—often caused by elevated pulmonary arterial pressure—is a chronic and progressive condition with particularly high mortality rates. Recent studies and our current findings suggest that components of Wild garlic (Allium ursinum, AU) may play a role in reducing blood [...] Read more.
Right-sided heart failure—often caused by elevated pulmonary arterial pressure—is a chronic and progressive condition with particularly high mortality rates. Recent studies and our current findings suggest that components of Wild garlic (Allium ursinum, AU) may play a role in reducing blood pressure, inhibiting angiotensin-converting enzyme (ACE), as well as improving right ventricle function in rabbit models with heart failure. We hypothesize that AU may mitigate cardiovascular damage caused by pulmonary arterial hypertension (PAH) and has value in the supplementary treatment of the complications of the disease. In this present investigation, PAH was induced by a single dose of monocrotaline (MCT) injection in Sprague-Dawley rats, and animals were divided into 4 treatment groups as follows: I. healthy control animals (Control group); II. pulmonary hypertensive rats (PAH group); III. pulmonary hypertensive rats + daily sildenafil treatment (Sildenafil group); and IV. pulmonary hypertensive rats + Wild garlic liophylisate-enriched chow (WGLL group), for 8 weeks. Echocardiographic measurements were obtained on the 0 and 8 weeks with fundamental and Doppler imaging. Isolated working heart method was used to determinate cardiac functions ex vivo after thoracotomy on the 8th week. Histological analyses were carried out on excised lung samples, and Western blot technique was used to determine Phosphodiesterase type 5 enzyme (PDE5) expression in both myocardial and pulmonary tissues. Our data demonstrate that right ventricle function measured by echocardiography was deteriorated in PAH animals compared to controls, which was counteracted by AU treatment. Isolated working heart measurements showed elevated aortic flow in WGLL group compared to PAH animals. Histological analysis revealed dramatic increase in medial wall thickness of pulmonary arteries harvested from PAH animals, but arteries of animals in sildenafil- and WGLL-treated groups showed physiological status. Our results suggest that bioactive compounds in Allium ursinum could have beneficial effects in pulmonary hypertension. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1036 KiB  
Article
Loss of Bone Mineral Density Associated with Age in Male Rats Fed on Sunflower Oil Is Avoided by Virgin Olive Oil Intake or Coenzyme Q Supplementation
by Alfonso Varela-López, Julio J. Ochoa, José M. Llamas-Elvira, Magdalena López-Frías, Elena Planells, Lorenza Speranza, Maurizio Battino and José L. Quiles
Int. J. Mol. Sci. 2017, 18(7), 1397; https://doi.org/10.3390/ijms18071397 - 29 Jun 2017
Cited by 19 | Viewed by 5164
Abstract
The role of dietary fat unsaturation and the supplementation of coenzyme Q have been evaluated in relation to bone health. Male Wistar rats were maintained for 6 or 24 months on two diets varying in the fat source, namely virgin olive oil, rich [...] Read more.
The role of dietary fat unsaturation and the supplementation of coenzyme Q have been evaluated in relation to bone health. Male Wistar rats were maintained for 6 or 24 months on two diets varying in the fat source, namely virgin olive oil, rich in monounsaturated fatty acids, or sunflower oil, rich in n-6 polyunsaturated fatty acids. Both dietary fats were supplemented or not with coenzyme Q10 (CoQ10). Bone mineral density (BMD) was evaluated in the femur. Serum levels of osteocalcin, osteopontin, receptor activator of nuclear factor κB ligand (RANKL), osteoprotegerin (OPG), adrenocorticotropin (ACTH) and parathyroid hormone (PTH), as well as urinary F2-isoprostanes were measured. Aged animals fed on virgin olive oil showed higher BMD than those fed on sunflower oil. In addition, CoQ10 prevented the age-related decline in BMD in animals fed on sunflower oil. Urinary F2-isoprostanes analysis showed that sunflower oil led to the highest oxidative status in old animals, which was avoided by supplementation with CoQ10. In conclusion, lifelong feeding on virgin olive oil or the supplementation of sunflower oil on CoQ10 prevented, at least in part mediated by a low oxidative stress status, the age-related decrease in BMD found in sunflower oil fed animals. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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5354 KiB  
Article
The Roles of Reactive Oxygen Species and Nitric Oxide in Perfluorooctanoic Acid-Induced Developmental Cardiotoxicity and l-Carnitine Mediated Protection
by Meng Zhao, Qixiao Jiang, Wencheng Wang, Min Geng, Meng Wang, Yantao Han and Chunbo Wang
Int. J. Mol. Sci. 2017, 18(6), 1229; https://doi.org/10.3390/ijms18061229 - 8 Jun 2017
Cited by 15 | Viewed by 5988
Abstract
Perfluorooctanoic acid (PFOA) is an environmental contaminant that could induce developmental cardiotoxicity in a chicken embryo, which may be alleviated by l-carnitine. To explore the roles of reactive oxygen species (ROS) and nitric oxide (NO) in such changes and the potential effects [...] Read more.
Perfluorooctanoic acid (PFOA) is an environmental contaminant that could induce developmental cardiotoxicity in a chicken embryo, which may be alleviated by l-carnitine. To explore the roles of reactive oxygen species (ROS) and nitric oxide (NO) in such changes and the potential effects of l-carnitine, fertile chicken eggs were exposed to PFOA via an air cell injection, with or without l-carnitine co-treatment. The ROS and NO levels in chicken embryo hearts were determined with electron spin resonance (ESR), and the protein levels of the nuclear factor κ-light chain-enhancer of activated B cells (NF-κB) p65 and inducible nitric oxide synthase (iNOS) in chicken embryo hearts were assessed with western blotting. The results of ESR indicated that PFOA exposure induced an elevation in the ROS levels in ED19 chicken embryo hearts and hatchling chicken hearts, while l-carnitine could alleviate such changes. Meanwhile, increased NO levels were observed in ED19 embryo hearts and hatchling hearts following PFOA exposure, while l-carnitine co-treatment exerted modulatory effects. Western blotting revealed that p65 translocation in ED19 embryo hearts and hatchling hearts was enhanced by PFOA, while l-carnitine co-treatment alleviated such changes. iNOS expression levels in ED19 embryo hearts followed the same pattern as NO levels, while a suppression of expression was observed in hatchling hearts exposed to PFOA. ROS/NF-κB p65 and iNOS/NO seem to be involved in the late stage (ED19 and post hatch) of PFOA-induced developmental cardiotoxicity in a chicken embryo. l-carnitine could exert anti-oxidant and NO modulatory effects in the developing chicken embryo hearts, which likely contribute to its cardioprotective effects. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1261 KiB  
Article
Molecular Pathways Involved in the Amelioration of Myocardial Injury in Diabetic Rats by Kaempferol
by Kapil Suchal, Salma Malik, Sana Irfan Khan, Rajiv Kumar Malhotra, Sameer N. Goyal, Jagriti Bhatia, Shreesh Ojha and Dharamvir Singh Arya
Int. J. Mol. Sci. 2017, 18(5), 1001; https://doi.org/10.3390/ijms18051001 - 15 May 2017
Cited by 88 | Viewed by 7223
Abstract
There is growing evidence that chronic hyperglycemia leads to the formation of advanced glycation end products (AGEs) which exerts its effect via interaction with the receptor for advanced glycation end products (RAGE). AGE-RAGE activation results in oxidative stress and inflammation. It is well [...] Read more.
There is growing evidence that chronic hyperglycemia leads to the formation of advanced glycation end products (AGEs) which exerts its effect via interaction with the receptor for advanced glycation end products (RAGE). AGE-RAGE activation results in oxidative stress and inflammation. It is well known that this mechanism is involved in the pathogenesis of cardiovascular disease in diabetes. Kaempferol, a dietary flavonoid, is known to possess antioxidant, anti-apoptotic, and anti-inflammatory activities. However, little is known about the effect of kaempferol on myocardial ischemia-reperfusion (IR) injury in diabetic rats. Diabetes was induced in male albino Wistar rats using streptozotocin (70 mg/kg; i.p.), and rats with glucose level >250 mg/dL were considered as diabetic. Diabetic rats were treated with vehicle (2 mL/kg; i.p.) and kaempferol (20 mg/kg; i.p.) daily for a period of 28 days and on the 28th day, ischemia was produced by one-stage ligation of the left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. After completion of surgery, rats were sacrificed and the heart tissue was processed for biochemical, morphological, and molecular studies. Kaempferol pretreatment significantly reduced hyperglycemia, maintained hemodynamic function, suppressed AGE-RAGE axis activation, normalized oxidative stress, and preserved morphological alterations. In addition, there was decreased level of inflammatory markers (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and NF-κB), inhibition of active c-Jun N-terminal kinase (JNK) and p38 proteins, and activation of Extracellular signal regulated kinase 1/2 (ERK1/2) a prosurvival kinase. Furthermore, it also attenuated apoptosis by reducing the expression of pro-apoptotic proteins (Bax and Caspase-3), Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cells, and increasing the level of anti-apoptotic protein (Bcl-2). In conclusion, kaempferol attenuated myocardial ischemia-reperfusion injury in diabetic rats by reducing AGE-RAGE/ mitogen activated protein kinase (MAPK) induced oxidative stress and inflammation. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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4184 KiB  
Article
Folic Acid Supplementation Delays Atherosclerotic Lesion Development by Modulating MCP1 and VEGF DNA Methylation Levels In Vivo and In Vitro
by Shanshan Cui, Wen Li, Xin Lv, Pengyan Wang, Yuxia Gao and Guowei Huang
Int. J. Mol. Sci. 2017, 18(5), 990; https://doi.org/10.3390/ijms18050990 - 5 May 2017
Cited by 40 | Viewed by 7003
Abstract
The pathogenesis of atherosclerosis has been partly acknowledged to result from aberrant epigenetic mechanisms. Accordingly, low folate levels are considered to be a contributing factor to promoting vascular disease because of deregulation of DNA methylation. We hypothesized that increasing the levels of folic [...] Read more.
The pathogenesis of atherosclerosis has been partly acknowledged to result from aberrant epigenetic mechanisms. Accordingly, low folate levels are considered to be a contributing factor to promoting vascular disease because of deregulation of DNA methylation. We hypothesized that increasing the levels of folic acid may act via an epigenetic gene silencing mechanism to ameliorate atherosclerosis. Here, we investigated the atheroprotective effects of folic acid and the resultant methylation status in high-fat diet-fed ApoE knockout mice and in oxidized low-density lipoprotein-treated human umbilical vein endothelial cells. We analyzed atherosclerotic lesion histology, folate concentration, homocysteine concentration, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), and DNA methyltransferase activity, as well as monocyte chemotactic protein-1 (MCP1) and vascular endothelial growth factor (VEGF) expression and promoter methylation. Folic acid reduced atherosclerotic lesion size in ApoE knockout mice. The underlying folic acid protective mechanism appears to operate through regulating the normal homocysteine state, upregulating the SAM: SAH ratio, elevating DNA methyltransferase activity and expression, altering MCP1 and VEGF promoter methylation, and inhibiting MCP1 and VEGF expression. We conclude that folic acid supplementation effectively prevented atherosclerosis by modifying DNA methylation through the methionine cycle, improving DNA methyltransferase activity and expression, and thus changing the expression of atherosclerosis-related genes. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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5420 KiB  
Article
Protective Effect of Fragaria ananassa Crude Extract on Cadmium-Induced Lipid Peroxidation, Antioxidant Enzymes Suppression, and Apoptosis in Rat Testes
by Mohammed I. Y. Elmallah, Manal F. Elkhadragy, Ebtesam M. Al-Olayan and Ahmed E. Abdel Moneim
Int. J. Mol. Sci. 2017, 18(5), 957; https://doi.org/10.3390/ijms18050957 - 5 May 2017
Cited by 72 | Viewed by 6875
Abstract
Cadmium is a deleterious environmental pollutant that threats both animals and human health. Oxidative stress and elevated levels of reactive oxygen species (ROS) have recently been reported to be the main cause of cellular damage as a result of cadmium exposure. We investigate, [...] Read more.
Cadmium is a deleterious environmental pollutant that threats both animals and human health. Oxidative stress and elevated levels of reactive oxygen species (ROS) have recently been reported to be the main cause of cellular damage as a result of cadmium exposure. We investigate, here, the protective effect of strawberry crude extracts on cadmium-induced oxidative damage of testes in rats. Four groups (n = 8) of 32 adult male Wistar rats weighing 160–180 g were used. The control group received 0.9% saline solution all over the experimental period (5 days). Group 2 was intraperitoneally injected with 6.5 mg/kg CdCl2. Group 3 was provided only with an oral administration of strawberry methanolic extract (SME) at a dose of 250 mg/kg. Group 4 was treated with SME before cadmium injection with the same mentioned doses. It was shown that cadmium exposure results in a significant decrease in both relative testicular weight and serum testosterone level. Analyzing the oxidative damaging effect of cadmium on the testicular tissue revealed the induction of oxidative stress markers represented in the elevated level of lipid peroxidation (LPO), nitric oxide (NO), and a decrease in the reduced glutathione (GSH) content. Considering cadmium toxicity, the level of the antioxidant enzyme activities including catalase (CAT), superoxide dismutase (SOD2), glutathione peroxidase (GPx1), and glutathione reductase (GR) were markedly decreased. Moreover, gene expression analysis indicated significant upregulation of the pro-apoptotic proteins, bcl-2-associated-X-protein (BAX), and tumor necrosis factor-α (TNFA) in response to cadmium intoxication, while significant downregulation of the anti-apoptotic, B-cell lymphoma 2 (BCL2) gene was detected. Immunohistochemistry of the testicular tissue possessed positive immunostaining for the increased level of TNF-α, but decreased number of proliferating cell nuclear antigen (PCNA) stained cells. Administration of SME debilitated the deleterious effect of cadmium via reduction of both LPO and NO levels followed by a significant enhancement in the gene expression level of CAT, SOD2, GPX1, GR, nuclear factor-erythroid 2-related factor 2 (NFE2L2), heme oxygenase-1 (HMOX1), Bcl-2, and PCNA. In addition, the SME treated group revealed a significant increase in the level of testosterone and GSH accompanied by a marked decrease in the gene expression level of Bax and TNF-α. In terms of the summarized results, the SME of Fragaria ananassa has a protective effect against cadmium-induced oxidative damage of testes. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1666 KiB  
Article
Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation
by Sara Franceschelli, Mirko Pesce, Alessio Ferrone, Daniela Maria Pia Gatta, Antonia Patruno, Maria Anna De Lutiis, José Luis Quiles, Alfredo Grilli, Mario Felaco and Lorenza Speranza
Int. J. Mol. Sci. 2017, 18(4), 690; https://doi.org/10.3390/ijms18040690 - 23 Mar 2017
Cited by 57 | Viewed by 5877
Abstract
Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the [...] Read more.
Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the effect of LicoC on the inflammatory response that characterizes septic myocardial dysfunction is poorly understood. The aim of this study was to determine whether LicoC exhibits anti-inflammatory properties on H9c2 cells that are stimulated with lipopolysaccharide. Our results have shown that LicoC treatment represses nuclear factor-κB (NF-κB) translocation and several downstream molecules, such as inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, LicoC has upregulated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signaling pathway. Finally, 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002), a specific PI3K inhibitor, blocked the protective effects of LicoC. These findings indicate that LicoC plays a pivotal role in cardiac dysfunction in sepsis-induced inflammation. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1541 KiB  
Article
Combined Effects of Curcumin and Lycopene or Bixin in Yoghurt on Inhibition of LDL Oxidation and Increases in HDL and Paraoxonase Levels in Streptozotocin-Diabetic Rats
by Renata Pires Assis, Carlos Alberto Arcaro, Vânia Ortega Gutierres, Juliana Oriel Oliveira, Paulo Inácio Costa, Amanda Martins Baviera and Iguatemy Lourenço Brunetti
Int. J. Mol. Sci. 2017, 18(4), 332; https://doi.org/10.3390/ijms18040332 - 23 Mar 2017
Cited by 73 | Viewed by 8394
Abstract
Combination therapy using natural antioxidants to manage diabetes mellitus and its complications is an emerging trend. The aim of this study was to investigate the changes promoted by treatment of streptozotocin (STZ)-diabetic rats with yoghurt enriched with the bioactives curcumin, lycopene, or bixin [...] Read more.
Combination therapy using natural antioxidants to manage diabetes mellitus and its complications is an emerging trend. The aim of this study was to investigate the changes promoted by treatment of streptozotocin (STZ)-diabetic rats with yoghurt enriched with the bioactives curcumin, lycopene, or bixin (the latter two being carotenoids). Antioxidants were administered individually, or as mixtures, and biomarkers of metabolic and oxidative disturbances, particularly those associated with cardiovascular risk, were assessed. Treatment of STZ-diabetic rats with natural products individually decreased glycemia, triacylglycerol, total-cholesterol, oxidative stress biomarkers, including oxidized low-density lipoprotein (ox-LDL), and increased the activities of antioxidant enzymes. Individual carotenoids increased both high-density lipoprotein (HDL) and paraoxonase levels, whereas curcumin increased only paraoxonase. Treatments with mixtures of curcumin and lycopene or bixin had combined effects, decreasing biomarkers of carbohydrate and lipid disturbances (curcumin effect), increasing the HDL levels (carotenoids effects) and mitigating oxidative stress (curcumin and carotenoids effects). The combined effects also led to prevention of the LDL oxidation, thereby mitigating the cardiovascular risk in diabetes. These findings provide evidence for the beneficial effect of curcumin and carotenoid mixtures as a supplementation having antioxidant and antiatherogenic potentials, thus appearing as an interesting strategy to be studied as a complementary therapy for diabetic complications. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Review

Jump to: Research

25 pages, 1638 KiB  
Review
Reactive Oxygen Species Produced by 5-Aminolevulinic Acid Photodynamic Therapy in the Treatment of Cancer
by Pamela Pignatelli, Samia Umme, Domenica Lucia D’Antonio, Adriano Piattelli and Maria Cristina Curia
Int. J. Mol. Sci. 2023, 24(10), 8964; https://doi.org/10.3390/ijms24108964 - 18 May 2023
Cited by 20 | Viewed by 3109
Abstract
Cancer is the leading cause of death worldwide and several anticancer therapies take advantage of the ability of reactive oxygen species to kill cancer cells. Added to this is the ancient hypothesis that light alone can be used to kill cancer cells. 5-aminolevulinic [...] Read more.
Cancer is the leading cause of death worldwide and several anticancer therapies take advantage of the ability of reactive oxygen species to kill cancer cells. Added to this is the ancient hypothesis that light alone can be used to kill cancer cells. 5-aminolevulinic acid-photodynamic therapy (5-ALA-PDT) is a therapeutic option for a variety of cutaneous and internal malignancies. PDT uses a photosensitizer that, activated by light in the presence of molecule oxygen, forms ROS, which are responsible for the apoptotic activity of the malignant tissues. 5-ALA is usually used as an endogenous pro-photosensitizer because it is converted to Protoporphyrin IX (PpIX), which enters into the process of heme synthesis and contextually becomes a photosensitizer, radiating a red fluorescent light. In cancer cells, the lack of the ferrochelatase enzyme leads to an accumulation of PpIX and consequently to an increased production of ROS. PDT has the benefit of being administered before or after chemotherapy, radiation, or surgery, without impairing the efficacy of these treatment techniques. Furthermore, sensitivity to PDT is unaffected by the negative effects of chemotherapy or radiation. This review focuses on the studies done so far on 5-ALA-PDT and its efficacy in the treatment of various cancer pathologies. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 3.0)
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21 pages, 798 KiB  
Review
Mitochondrial Aging and Senolytic Natural Products with Protective Potential
by Andrea Deledda, Emanuele Giordano, Fernanda Velluzzi, Giovanna Flore, Sara Franceschelli, Lorenza Speranza and Patrizio Ripari
Int. J. Mol. Sci. 2022, 23(24), 16219; https://doi.org/10.3390/ijms232416219 - 19 Dec 2022
Cited by 11 | Viewed by 10710
Abstract
Living organisms do not disregard the laws of thermodynamics and must therefore consume energy for their survival. In this way, cellular energy exchanges, which aim above all at the production of ATP, a fundamental molecule used by the cell for its metabolisms, favor [...] Read more.
Living organisms do not disregard the laws of thermodynamics and must therefore consume energy for their survival. In this way, cellular energy exchanges, which aim above all at the production of ATP, a fundamental molecule used by the cell for its metabolisms, favor the formation of waste products that, if not properly disposed of, can contribute to cellular aging and damage. Numerous genes have been linked to aging, with some favoring it (gerontogenes) and others blocking it (longevity pathways). Animal model studies have shown that calorie restriction (CR) may promote longevity pathways, but given the difficult application of CR in humans, research is investigating the use of CR-mimetic substances capable of producing the same effect. These include some phytonutrients such as oleuropein, hydroxytyrosol, epigallo-catechin-gallate, fisetin, quercetin, and curcumin and minerals such as magnesium and selenium. Some of them also have senolytic effects, which promote the apoptosis of defective cells that accumulate over the years (senescent cells) and disrupt normal metabolism. In this article, we review the properties of these natural elements that can promote a longer and healthier life. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 3.0)
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21 pages, 1804 KiB  
Review
Caffeine and Its Antioxidant Properties—It Is All about Dose and Source
by Bianca-Eugenia Ősz, George Jîtcă, Ruxandra-Emilia Ștefănescu, Amalia Pușcaș, Amelia Tero-Vescan and Camil-Eugen Vari
Int. J. Mol. Sci. 2022, 23(21), 13074; https://doi.org/10.3390/ijms232113074 - 28 Oct 2022
Cited by 37 | Viewed by 9236
Abstract
Caffeine is the most frequently used substance with a central nervous system stimulant effect, but its consumption is most often due to the intake of foods and drinks that contain it (coffee, tea, chocolate, food supplements with plant extracts of Guarana, Mate herba [...] Read more.
Caffeine is the most frequently used substance with a central nervous system stimulant effect, but its consumption is most often due to the intake of foods and drinks that contain it (coffee, tea, chocolate, food supplements with plant extracts of Guarana, Mate herba, Cola nuts). Due to its innocuity, caffeine is a safe xanthine alkaloid for human consumption in a wide range of doses, being used for its central nervous stimulating effect, lipolytic and diuresis-enhancing properties, but also as a permitted ergogenic compound in athletes. In addition to the mechanisms that explain the effects of caffeine on the targeted organ, there are many proposed mechanisms by which this substance would have antioxidant effects. As such, its consumption prevents the occurrence/progression of certain neurodegenerative diseases as well as other medical conditions associated with increased levels of reactive oxygen or nitrogen species. However, most studies that have assessed the beneficial effects of caffeine have used pure caffeine. The question, therefore, arises whether the daily intake of caffeine from food or drink has similar benefits, considering that in foods or drinks with a high caffeine content, there are other substances that could interfere with this action, either by potentiating or decreasing its antioxidant capacity. Natural sources of caffeine often combine plant polyphenols (phenol-carboxylic acids, catechins) with known antioxidant effects; however, stimulant drinks and dietary supplements often contain sugars or artificial sweeteners that can significantly reduce the effects of caffeine on oxidative stress. The objective of this review is to clarify the effects of caffeine in modulating oxidative stress and assess these benefits, considering the source and the dose administered. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 3.0)
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19 pages, 986 KiB  
Review
Early-Life Programming and Reprogramming of Adult Kidney Disease and Hypertension: The Interplay between Maternal Nutrition and Oxidative Stress
by Chien-Ning Hsu and You-Lin Tain
Int. J. Mol. Sci. 2020, 21(10), 3572; https://doi.org/10.3390/ijms21103572 - 18 May 2020
Cited by 22 | Viewed by 4108
Abstract
Kidney disease and hypertension both have attained the status of a global pandemic. Altered renal programming resulting in kidney disease and hypertension can begin in utero. Maternal suboptimal nutrition and oxidative stress have important implications in renal programming, while specific antioxidant nutrient supplementations [...] Read more.
Kidney disease and hypertension both have attained the status of a global pandemic. Altered renal programming resulting in kidney disease and hypertension can begin in utero. Maternal suboptimal nutrition and oxidative stress have important implications in renal programming, while specific antioxidant nutrient supplementations may serve as reprogramming strategies to prevent kidney disease and hypertension of developmental origins. This review aims to summarize current knowledge on the interplay of maternal nutrition and oxidative stress in response to early-life insults and its impact on developmental programming of kidney disease and hypertension, covering two aspects. Firstly, we present the evidence from animal models supporting the implication of oxidative stress on adult kidney disease and hypertension programmed by suboptimal maternal nutrition. In the second part, we document data on specific antioxidant nutrients as reprogramming strategies to protect adult offspring against kidney disease and hypertension from developmental origins. Research into the prevention of kidney disease and hypertension that begin early in life will have profound implications for future health. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 2.0)
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17 pages, 852 KiB  
Review
Tea and Its Components Prevent Cancer: A Review of the Redox-Related Mechanism
by Xiangbing Mao, Xiangjun Xiao, Daiwen Chen, Bing Yu and Jun He
Int. J. Mol. Sci. 2019, 20(21), 5249; https://doi.org/10.3390/ijms20215249 - 23 Oct 2019
Cited by 29 | Viewed by 4827
Abstract
Cancer is a worldwide epidemic and represents a major threat to human health and survival. Reactive oxygen species (ROS) play a dual role in cancer cells, which includes both promoting and inhibiting carcinogenesis. Tea remains one of the most prevalent beverages consumed due [...] Read more.
Cancer is a worldwide epidemic and represents a major threat to human health and survival. Reactive oxygen species (ROS) play a dual role in cancer cells, which includes both promoting and inhibiting carcinogenesis. Tea remains one of the most prevalent beverages consumed due in part to its anti- or pro-oxidative properties. The active compounds in tea, particularly tea polyphenols, can directly or indirectly scavenge ROS to reduce oncogenesis and cancerometastasis. Interestingly, the excessive levels of ROS induced by consuming tea could induce programmed cell death (PCD) or non-PCD of cancer cells. On the basis of illustrating the relationship between ROS and cancer, the current review discusses the composition and efficacy of tea including the redox-relative (including anti-oxidative and pro-oxidative activity) mechanisms and their role along with other components in preventing and treating cancer. This information will highlight the basis for the clinical utilization of tea extracts in the prevention or treatment of cancer in the future. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease 2.0)
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585 KiB  
Review
Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders
by Simona Dinicola, Mirko Minini, Vittorio Unfer, Roberto Verna, Alessandra Cucina and Mariano Bizzarri
Int. J. Mol. Sci. 2017, 18(10), 2187; https://doi.org/10.3390/ijms18102187 - 20 Oct 2017
Cited by 82 | Viewed by 14804
Abstract
Communities eating a western-like diet, rich in fat, sugar and significantly deprived of fibers, share a relevant increased risk of both metabolic and cancerous diseases. Even more remarkable is that a low-fiber diet lacks some key components—as phytates and inositols—for which a mechanistic [...] Read more.
Communities eating a western-like diet, rich in fat, sugar and significantly deprived of fibers, share a relevant increased risk of both metabolic and cancerous diseases. Even more remarkable is that a low-fiber diet lacks some key components—as phytates and inositols—for which a mechanistic link has been clearly established in the pathogenesis of both cancer and metabolic illness. Reduced bioavailability of inositol in living organisms could arise from reduced food supply or from metabolism deregulation. Inositol deregulation has been found in a number of conditions mechanistically and epidemiologically associated to high-glucose diets or altered glucose metabolism. Indeed, high glucose levels hinder inositol availability by increasing its degradation and by inhibiting both myo-Ins biosynthesis and absorption. These underappreciated mechanisms may likely account for acquired, metabolic deficiency in inositol bioavailability. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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759 KiB  
Review
Dietary Modulation of Oxidative Stress in Alzheimer’s Disease
by Arjun Thapa and Nick J. Carroll
Int. J. Mol. Sci. 2017, 18(7), 1583; https://doi.org/10.3390/ijms18071583 - 21 Jul 2017
Cited by 71 | Viewed by 10780
Abstract
Cells generate unpaired electrons, typically via oxygen- or nitrogen-based by-products during normal cellular respiration and under stressed situations. These pro-oxidant molecules are highly unstable and may oxidize surrounding cellular macromolecules. Under normal conditions, the reactive oxygen or nitrogen species can be beneficial to [...] Read more.
Cells generate unpaired electrons, typically via oxygen- or nitrogen-based by-products during normal cellular respiration and under stressed situations. These pro-oxidant molecules are highly unstable and may oxidize surrounding cellular macromolecules. Under normal conditions, the reactive oxygen or nitrogen species can be beneficial to cell survival and function by destroying and degrading pathogens or antigens. However, excessive generation and accumulation of the reactive pro-oxidant species over time can damage proteins, lipids, carbohydrates, and nucleic acids. Over time, this oxidative stress can contribute to a range of aging-related degenerative diseases such as cancer, diabetes, macular degeneration, and Alzheimer’s, and Parkinson’s diseases. It is well accepted that natural compounds, including vitamins A, C, and E, β-carotene, and minerals found in fruits and vegetables are powerful anti-oxidants that offer health benefits against several different oxidative stress induced degenerative diseases, including Alzheimer’s disease (AD). There is increasing interest in developing anti-oxidative therapeutics to prevent AD. There are contradictory and inconsistent reports on the possible benefits of anti-oxidative supplements; however, fruits and vegetables enriched with multiple anti-oxidants (e.g., flavonoids and polyphenols) and minerals may be highly effective in attenuating the harmful effects of oxidative stress. As the physiological activation of either protective or destructive pro-oxidant behavior remains relatively unclear, it is not straightforward to relate the efficacy of dietary anti-oxidants in disease prevention. Here, we review oxidative stress mediated toxicity associated with AD and highlight the modulatory roles of natural dietary anti-oxidants in preventing AD. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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3462 KiB  
Review
Correlation between Oxidative Stress, Nutrition, and Cancer Initiation
by Subbroto Kumar Saha, Soo Bin Lee, Jihye Won, Hye Yeon Choi, Kyeongseok Kim, Gwang-Mo Yang, Ahmed Abdal Dayem and Ssang-goo Cho
Int. J. Mol. Sci. 2017, 18(7), 1544; https://doi.org/10.3390/ijms18071544 - 17 Jul 2017
Cited by 297 | Viewed by 21666
Abstract
Inadequate or excessive nutrient consumption leads to oxidative stress, which may disrupt oxidative homeostasis, activate a cascade of molecular pathways, and alter the metabolic status of various tissues. Several foods and consumption patterns have been associated with various cancers and approximately 30–35% of [...] Read more.
Inadequate or excessive nutrient consumption leads to oxidative stress, which may disrupt oxidative homeostasis, activate a cascade of molecular pathways, and alter the metabolic status of various tissues. Several foods and consumption patterns have been associated with various cancers and approximately 30–35% of the cancer cases are correlated with overnutrition or malnutrition. However, several contradictory studies are available regarding the association between diet and cancer risk, which remains to be elucidated. Concurrently, oxidative stress is a crucial factor for cancer progression and therapy. Nutritional oxidative stress may be induced by an imbalance between antioxidant defense and pro-oxidant load due to inadequate or excess nutrient supply. Oxidative stress is a physiological state where high levels of reactive oxygen species (ROS) and free radicals are generated. Several signaling pathways associated with carcinogenesis can additionally control ROS generation and regulate ROS downstream mechanisms, which could have potential implications in anticancer research. Cancer initiation may be modulated by the nutrition-mediated elevation in ROS levels, which can stimulate cancer initiation by triggering DNA mutations, damage, and pro-oncogenic signaling. Therefore, in this review, we have provided an overview of the relationship between nutrition, oxidative stress, and cancer initiation, and evaluated the impact of nutrient-mediated regulation of antioxidant capability against cancer therapy. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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313 KiB  
Review
Naturally Occurring Compounds: New Potential Weapons against Oxidative Stress in Chronic Kidney Disease
by Lorenzo Signorini, Simona Granata, Antonio Lupo and Gianluigi Zaza
Int. J. Mol. Sci. 2017, 18(7), 1481; https://doi.org/10.3390/ijms18071481 - 10 Jul 2017
Cited by 25 | Viewed by 5900
Abstract
Oxidative stress is a well-described imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense system of cells and tissues. The overproduction of free radicals damages all components of the cell (proteins, lipids, nucleic acids) and modifies their physiological functions. [...] Read more.
Oxidative stress is a well-described imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense system of cells and tissues. The overproduction of free radicals damages all components of the cell (proteins, lipids, nucleic acids) and modifies their physiological functions. As widely described, this condition is a biochemical hallmark of chronic kidney disease (CKD) and may dramatically influence the progression of renal impairment and the onset/development of major systemic comorbidities including cardiovascular diseases. This state is exacerbated by exposure of the body to uremic toxins and dialysis, a treatment that, although necessary to ensure patients’ survival, exposes cells to non-physiological contact with extracorporeal circuits and membranes with consequent mitochondrial and anti-redox cellular system alterations. Therefore, it is undeniable that counteracting oxidative stress machinery is a major pharmacological target in medicine/nephrology. As a consequence, in recent years several new naturally occurring compounds, administered alone or integrated with classical therapies and an appropriate lifestyle, have been proposed as therapeutic tools for CKD patients. In this paper, we reviewed the recent literature regarding the “pioneering” in vivo testing of these agents and their inclusion in small clinical trials performed in patients affected by CKD. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1042 KiB  
Review
Hypotheses on the Potential of Rice Bran Intake to Prevent Gastrointestinal Cancer through the Modulation of Oxidative Stress
by Bernard M. H. Law, Mary M. Y. Waye, Winnie K. W. So and Sek Ying Chair
Int. J. Mol. Sci. 2017, 18(7), 1352; https://doi.org/10.3390/ijms18071352 - 24 Jun 2017
Cited by 26 | Viewed by 7518
Abstract
Previous studies have suggested the potential involvement of oxidative stress in gastrointestinal cancers. In light of this, research efforts have been focused on the potential of dietary antioxidant intake to prevent gastrointestinal cancer through the modulation of oxidative stress. Rice bran, a by-product [...] Read more.
Previous studies have suggested the potential involvement of oxidative stress in gastrointestinal cancers. In light of this, research efforts have been focused on the potential of dietary antioxidant intake to prevent gastrointestinal cancer through the modulation of oxidative stress. Rice bran, a by-product of rice milling, has been shown to contain an abundance of phytochemicals, which are dietary antioxidants. To date, a number of studies have shown the antioxidative effect of rice bran intake, and some demonstrated that such an effect may contribute to gastrointestinal cancer prevention, largely through the antioxidative properties of rice bran phytochemicals. In addition, these phytochemicals were shown to provide protection against cancer through mechanisms linked to oxidative stress, including β-catenin-mediated cell proliferation and inflammation. The present article provides an overview of current evidence for the antioxidative properties of rice bran and its phytochemicals, and for the potential of such properties in cancer prevention through the oxidative-stress-linked mechanisms mentioned above. The article also highlights the need for an evaluation of the effectiveness of rice bran dietary interventions among cancer survivors in ameliorating oxidative stress and reducing the level of gastrointestinal cancer biomarkers, thereby establishing the potential of such interventions among these individuals in the prevention of cancer recurrence. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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936 KiB  
Review
Therapeutic Applications of Rose Hips from Different Rosa Species
by Inés Mármol, Cristina Sánchez-de-Diego, Nerea Jiménez-Moreno, Carmen Ancín-Azpilicueta and María Jesús Rodríguez-Yoldi
Int. J. Mol. Sci. 2017, 18(6), 1137; https://doi.org/10.3390/ijms18061137 - 25 May 2017
Cited by 126 | Viewed by 32714
Abstract
Rosa species, rose hips, are widespread wild plants that have been traditionally used as medicinal compounds for the treatment of a wide variety of diseases. The therapeutic potential of these plants is based on its antioxidant effects caused by or associated with its [...] Read more.
Rosa species, rose hips, are widespread wild plants that have been traditionally used as medicinal compounds for the treatment of a wide variety of diseases. The therapeutic potential of these plants is based on its antioxidant effects caused by or associated with its phytochemical composition, which includes ascorbic acid, phenolic compounds and healthy fatty acids among others. Over the last few years, medicinal interest in rose hips has increased as a consequence of recent research that has studied its potential application as a treatment for several diseases including skin disorders, hepatotoxicity, renal disturbances, diarrhoea, inflammatory disorders, arthritis, diabetes, hyperlipidaemia, obesity and cancer. In this review, the role of different species of Rosa in the prevention of treatment of various disorders related to oxidative stress, is examined, focusing on new therapeutic approaches from a molecular point of view. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1389 KiB  
Review
Interplay between Oxidative Stress and Nutrient Sensing Signaling in the Developmental Origins of Cardiovascular Disease
by You-Lin Tain and Chien-Ning Hsu
Int. J. Mol. Sci. 2017, 18(4), 841; https://doi.org/10.3390/ijms18040841 - 15 Apr 2017
Cited by 64 | Viewed by 7594
Abstract
Cardiovascular disease (CVD) presents a global health burden, despite recent advances in management. CVD can originate from early life by so-called “developmental origins of health and disease” (DOHaD). Epidemiological and experimental evidence supports that early-life insults can induce programming of later CVD. Underlying [...] Read more.
Cardiovascular disease (CVD) presents a global health burden, despite recent advances in management. CVD can originate from early life by so-called “developmental origins of health and disease” (DOHaD). Epidemiological and experimental evidence supports that early-life insults can induce programming of later CVD. Underlying the DOHaD concept, early intervention may offset programming process to prevent the development of CVD, namely reprogramming. Oxidative stress and nutrient sensing signals have been considered to be major mechanisms of cardiovascular programming, while the interplay between these two mechanisms have not been examined in detail. This review summarizes current evidence that supports the link between oxidative stress and nutrient sensing signaling to cardiovascular programming, with an emphasis on the l-arginine–asymmetric dimethylarginine (ADMA)–nitric oxide (NO) pathway. This review provides an overview of evidence from human studies supporting fetal programming of CVD, insight from animal models of cardiovascular programming and oxidative stress, impact of the l-arginine–ADMA–NO pathway in cardiovascular programming, the crosstalk between l-arginine metabolism and nutrient sensing signals, and application of reprogramming interventions to prevent the programming of CVD. A greater understanding of the mechanisms underlying cardiovascular programming is essential to developing early reprogramming interventions to combat the globally growing epidemic of CVD. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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247 KiB  
Review
Effects and Mechanisms of Fruit and Vegetable Juices on Cardiovascular Diseases
by Jie Zheng, Yue Zhou, Sha Li, Pei Zhang, Tong Zhou, Dong-Ping Xu and Hua-Bin Li
Int. J. Mol. Sci. 2017, 18(3), 555; https://doi.org/10.3390/ijms18030555 - 4 Mar 2017
Cited by 117 | Viewed by 35622
Abstract
Many studies have indicated that consumption of vegetables and fruits are positively related to lower incidence of several chronic noncommunicable diseases. Although composition of fruit and vegetable juices is different from that of the edible portion of fruits and vegetables, they contain polyphenols [...] Read more.
Many studies have indicated that consumption of vegetables and fruits are positively related to lower incidence of several chronic noncommunicable diseases. Although composition of fruit and vegetable juices is different from that of the edible portion of fruits and vegetables, they contain polyphenols and vitamins from fruits and vegetables. Drinking vegetable and fruit juices is very popular in many countries, and also an efficient way to improve consumption of fruits and vegetables. The studies showed that fruit and vegetable juices affect cardiovascular risk factors, such as lowering blood pressure and improving blood lipid profiles. The main mechanisms of action included antioxidant effects, improvement of the aspects of the cardiovascular system, inhibition of platelet aggregation, anti-inflammatory effects, and prevention of hyperhomocysteinemia. Drinking juices might be a potential way to improve cardiovascular health, especially mixtures of juices because they contain a variety of polyphenols, vitamins, and minerals from different fruits and vegetables. This review summarizes recent studies on the effects of fruit and vegetable juices on indicators of cardiovascular disease, and special attention is paid to the mechanisms of action. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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