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Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects

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

Deadline for manuscript submissions: closed (21 March 2021) | Viewed by 56686

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Dr. Antonio Mancini

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Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario A Gemelli IRCCS, Rome, Italy
Interests: adult growth hormone deficiency; oxidative stress in metabolic syndrome; pituitary disorders; male hypogonadism and infertility; policystic ovary syndrome
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Dr. Andrea Silvestrini

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Dipartimento di Scienze biotecnologiche di base, cliniche intensivologiche e perioperatorie, Università Cattolica del Sacro Cuore, Fondazione Policlinico Universitario A Gemelli IRCCS, Rome, Italy
Interests: biochemistry; oxidative stress; antioxidants; anthracycline
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress, as a mechanism underlying many clinical conditions, is well known and extensively reported in the literature. However, the complex inter-relationships between hormones, oxidative status, and inflammation are still far from being completely understood, since reciprocal and opposite influences can be exerted between these pathogenic factors in endocrine disease. Moreover, biochemical/biological data and application in clinical trials are still distant, requiring a more translational approach. The concept of what constitutes a hormone itself is changing, including virtually all organs and systems. Therefore, we aim to publish a Special Issue which can cover a wide spectrum, from biological to translational studies, in the field of endocrine and metabolic disorders.

This Special Issue seeks regular papers, reviews, and opinions, on topics including but not limited to:

Oxidative stress and endocrine disorders;

Oxidative stress and hormone metabolism;

Biomarkers and diagnostic methods in oxidative stress;

Antioxidant therapeutics;

Oxidative biomarkers.

All papers related to any aspect of oxidative stress physiology, biochemistry, and physiopathological bases in endocrine disease will be considered for this Special Issue.

Due to your extensive and eminent competence the field, it would be an honor to receive a contribution to give greater value to the present project.

Dr. Antonio Mancini
Dr. Andrea Silvestrini
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

antioxidants
radical species
nutraceutics
metabolic syndrome
endocrine glands
hormone metabolism
inflammation in endocrine disorders

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Related Special Issue

Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects 2.0 in International Journal of Molecular Sciences (19 articles)

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Research

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14 pages, 7712 KiB

Open AccessArticle

Local Epidermal Endocrine Estrogen Protects Human Melanocytes against Oxidative Stress, a Novel Insight into Vitiligo Pathology

by Asako Yamamoto, Lingli Yang, Yasutaka Kuroda, Jiao Guo, Lanting Teng, Daisuke Tsuruta and Ichiro Katayama

Int. J. Mol. Sci. 2021, 22(1), 269; https://doi.org/10.3390/ijms22010269 - 29 Dec 2020

Cited by 8 | Viewed by 3309

Abstract

As the outermost barrier of the body, skin is a major target of oxidative stress. In the brain, estrogen has been reported synthesized locally and protects neurons from oxidative stress. Here, we explored whether estrogen is also locally synthesized in the skin to protect from oxidative stress and whether aberrant local estrogen synthesis is involved in skin disorders. Enzymes and estrogen receptor expression in skin cells were examined first by quantitative real-time PCR and Western blot analyses. Interestingly, the estrogen synthesis enzyme was mainly localized in epidermal keratinocytes and estrogen receptors were mainly expressed in melanocytes among 13 kinds of cultured human skin cells. The most abundant estrogen synthesis enzyme expressed in the epidermis was 17β-hydroxysteroid dehydrogenase 1 (HSD17β1) localized in keratinocytes, and the most dominant estrogen receptor expressed in the epidermis was G protein-coupled estrogen receptor 1 (GPER1) in melanocytes. To investigate whether keratinocyte-derived estradiol could protect melanocytes from oxidative stress, cultured human primary epidermal melanocytes (HEMn-MPs) were treated with H₂O₂ in the presence or absence of 17β estradiol or co-cultured with HSD17β1 siRNA-transfected keratinocytes. Keratinocyte-derived estradiol exhibited protective effects against H₂O₂-induced cell death. Further, reduced expression of HSD17β1 in the epidermis of skin from vitiligo patients was observed compared to the skin from healthy donors or in the normal portions of the skin in vitiligo patients. Our results suggest a possible new target for interventions that may be used in combination with current therapies for patients with vitiligo. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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18 pages, 2435 KiB

Open AccessArticle

Coenzyme Q Depletion Reshapes MCF-7 Cells Metabolism

by Wenping Wang, Irene Liparulo, Nicola Rizzardi, Paola Bolignano, Natalia Calonghi, Christian Bergamini and Romana Fato

Int. J. Mol. Sci. 2021, 22(1), 198; https://doi.org/10.3390/ijms22010198 - 28 Dec 2020

Cited by 11 | Viewed by 3506

Abstract

Mitochondrial dysfunction plays a significant role in the metabolic flexibility of cancer cells. This study aimed to investigate the metabolic alterations due to Coenzyme Q depletion in MCF-7 cells. Method: The Coenzyme Q depletion was induced by competitively inhibiting with 4-nitrobenzoate the coq2 enzyme, which catalyzes one of the final reactions in the biosynthetic pathway of CoQ. The bioenergetic and metabolic characteristics of control and coenzyme Q depleted cells were investigated using polarographic and spectroscopic assays. The effect of CoQ depletion on cell growth was analyzed in different metabolic conditions. Results: we showed that cancer cells could cope from energetic and oxidative stress due to mitochondrial dysfunction by reshaping their metabolism. In CoQ depleted cells, the glycolysis was upregulated together with increased glucose consumption, overexpression of GLUT1 and GLUT3, as well as activation of pyruvate kinase (PK). Moreover, the lactate secretion rate was reduced, suggesting that the pyruvate flux was redirected, toward anabolic pathways. Finally, we found a different expression pattern in enzymes involved in glutamine metabolism, and TCA cycle in CoQ depleted cells in comparison to controls. Conclusion: This work elucidated the metabolic alterations in CoQ-depleted cells and provided an insightful understanding of cancer metabolism targeting. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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16 pages, 4343 KiB

Open AccessArticle

Deletion of Thioredoxin-Interacting Protein (TXNIP) Abrogates High Fat Diet-Induced Retinal Leukostasis, Barrier Dysfunction and Microvascular Degeneration in a Mouse Obesity Model

by Islam N. Mohamed, Nader Sheibani and Azza B. El-Remessy

Int. J. Mol. Sci. 2020, 21(11), 3983; https://doi.org/10.3390/ijms21113983 - 1 Jun 2020

Cited by 10 | Viewed by 3029

Abstract

We have shown that a high fat diet (HFD) induces the activation of retinal NOD-like receptor protein (NLRP3)-inflammasome that is associated with enhanced expression and interaction with thioredoxin-interacting protein (TXNIP). Here, the specific contribution of TXNIP and the impact of HFD on retinal leukostasis, barrier dysfunction and microvascular degeneration were investigated. Wild-type (WT) and TXNIP knockout (TKO) mice were fed with normal diet or 60% HFD for 8–18 weeks. TXNIP was overexpressed or silenced in human retinal endothelial cells (REC). At 8 weeks, HFD significantly induced retinal leukostasis and breakdown of the blood–retina barrier in WT mice, but not in TKO mice. In parallel, HFD also induced retinal expression of adhesion molecules and cleaved IL-1β in WT mice, which were also abrogated in TKO mice. In culture, TXNIP overexpression induced NLRP3, IL-1β, and adhesion molecules expression, while TXNIP silencing inhibited them. Blocking the IL-1β receptor significantly suppressed TXNIP-induced expression of NLRP3-inflammasome and adhesion molecules in HREC. Ex-vivo assay showed that leukocytes isolated from WT-HFD, but not from TKO-HFD, induced leukostasis and cell death. At 18 weeks, HFD triggered development of degenerated (acellular) capillaries and decreased branching density in WT but not in TKO mice. Together, HFD-induced obesity triggered early retinal leukostasis and microvascular dysfunction at least in part via TXNIP-NLRP3-inflammasome activation. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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Review

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13 pages, 547 KiB

Open AccessReview

The Role of Resveratrol Administration in Human Obesity

by Laura M. Mongioì, Sandro La Vignera, Rossella Cannarella, Laura Cimino, Michele Compagnone, Rosita A. Condorelli and Aldo E. Calogero

Int. J. Mol. Sci. 2021, 22(9), 4362; https://doi.org/10.3390/ijms22094362 - 22 Apr 2021

Cited by 40 | Viewed by 4539

Abstract

Obesity is a widespread disease that is associated with numerous and serious comorbidities. These include metabolic syndrome, diabetes mellitus, cardiovascular-cerebrovascular disease, hypertension, obstructive sleep apnea syndrome, cancer, and sexual and hormonal disorders. The treatment of obesity has therefore become a goal of great clinical and social relevance. Among the therapeutic strategies against obesity, resveratrol has aroused great interest. This polyphenol has anticancer and antioxidant properties and cytoprotective and anti-inflammatory effects. Other favorable effects attributed to resveratrol are anti-lipid, anti-aging, anti-bacterial, anti-viral, and neuroprotective actions. Administration of resveratrol appears to improve the metabolic profile in obese and/or insulin-resistant patients. This article aims to review the main results of clinical studies evaluating the effects of administering resveratrol alone in overweight/obese patients. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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26 pages, 1440 KiB

Open AccessReview

Oxidative Stress, Plant Natural Antioxidants, and Obesity

by Israel Pérez-Torres, Vicente Castrejón-Téllez, María Elena Soto, María Esther Rubio-Ruiz, Linaloe Manzano-Pech and Verónica Guarner-Lans

Int. J. Mol. Sci. 2021, 22(4), 1786; https://doi.org/10.3390/ijms22041786 - 11 Feb 2021

Cited by 220 | Viewed by 12714

Abstract

Oxidative stress is important in the pathophysiology of obesity, altering regulatory factors of mitochondrial activity, modifying the concentration of inflammation mediators associated with a large number and size of adipocytes, promoting lipogenesis, stimulating differentiation of preadipocytes to mature adipocytes, and regulating the energy balance in hypothalamic neurons that control appetite. This review discusses the participation of oxidative stress in obesity and the important groups of compounds found in plants with antioxidant properties, which include (a) polyphenols such as phenolic acids, stilbenes, flavonoids (flavonols, flavanols, anthocyanins, flavanones, flavones, flavanonols, and isoflavones), and curcuminoids (b) carotenoids, (c) capsaicinoids and casinoids, (d) isothiocyanates, (e) catechins, and (f) vitamins. Examples are analyzed, such as resveratrol, quercetin, curcumin, ferulic acid, phloretin, green tea, Hibiscus Sabdariffa, and garlic. The antioxidant activities of these compounds depend on their activities as reactive oxygen species (ROS) scavengers and on their capacity to prevent the activation of NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells), and reduce the expression of target genes, including those participating in inflammation. We conclude that natural compounds have therapeutic potential for diseases mediated by oxidative stress, particularly obesity. Controlled and well-designed clinical trials are still necessary to better know the effects of these compounds. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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17 pages, 1037 KiB

Open AccessReview

Oxidative Stress and Low-Grade Inflammation in Polycystic Ovary Syndrome: Controversies and New Insights

by Antonio Mancini, Carmine Bruno, Edoardo Vergani, Claudia d’Abate, Elena Giacchi and Andrea Silvestrini

Int. J. Mol. Sci. 2021, 22(4), 1667; https://doi.org/10.3390/ijms22041667 - 7 Feb 2021

Cited by 81 | Viewed by 10171

Abstract

The pathophysiology of Polycystic Ovary Syndrome (PCOS) is quite complex and different mechanisms could contribute to hyperandrogenism and anovulation, which are the main features of the syndrome. Obesity and insulin-resistance are claimed as the principal factors contributing to the clinical presentation; in normal weight PCOS either, increased visceral adipose tissue has been described. However, their role is still debated, as debated are the biochemical markers linked to obesity per se. Oxidative stress (OS) and low-grade inflammation (LGI) have recently been a matter of researcher attention; they can influence each other in a reciprocal vicious cycle. In this review, we summarize the main mechanism of radical generation and the link with LGI. Furthermore, we discuss papers in favor or against the role of obesity as the first pathogenetic factor, and show how OS itself, on the contrary, can induce obesity and insulin resistance; in particular, the role of GH-IGF-1 axis is highlighted. Finally, the possible consequences on vitamin D synthesis and activation on the immune system are briefly discussed. This review intends to underline the key role of oxidative stress and low-grade inflammation in the physiopathology of PCOS, they can cause or worsen obesity, insulin-resistance, vitamin D deficiency, and immune dyscrasia, suggesting an inverse interaction to what is usually considered. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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23 pages, 1374 KiB

Open AccessReview

Immunity as Cornerstone of Non-Alcoholic Fatty Liver Disease: The Contribution of Oxidative Stress in the Disease Progression

by Marcello Dallio, Moris Sangineto, Mario Romeo, Rosanna Villani, Antonino Davide Romano, Carmelina Loguercio, Gaetano Serviddio and Alessandro Federico

Int. J. Mol. Sci. 2021, 22(1), 436; https://doi.org/10.3390/ijms22010436 - 4 Jan 2021

Cited by 43 | Viewed by 6245

Abstract

Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome and has become the major cause of chronic liver disease, especially in western countries. NAFLD encompasses a wide spectrum of hepatic histological alterations, from simple steatosis to steatohepatitis and cirrhosis with a potential development of hepatocellular carcinoma. Non-alcoholic steatohepatitis (NASH) is characterized by lobular inflammation and fibrosis. Several studies reported that insulin resistance, redox unbalance, inflammation, and lipid metabolism dysregulation are involved in NAFLD progression. However, the mechanisms beyond the evolution of simple steatosis to NASH are not clearly understood yet. Recent findings suggest that different oxidized products, such as lipids, cholesterol, aldehydes and other macromolecules could drive the inflammation onset. On the other hand, new evidence indicates innate and adaptive immunity activation as the driving force in establishing liver inflammation and fibrosis. In this review, we discuss how immunity, triggered by oxidative products and promoting in turn oxidative stress in a vicious cycle, fuels NAFLD progression. Furthermore, we explored the emerging importance of immune cell metabolism in determining inflammation, describing the potential application of trained immune discoveries in the NASH pathological context. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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9 pages, 221 KiB

Open AccessReview

Hyperhomocysteinemia: Focus on Endothelial Damage as a Cause of Erectile Dysfunction

by Gianmaria Salvio, Alessandro Ciarloni, Melissa Cutini and Giancarlo Balercia

Int. J. Mol. Sci. 2021, 22(1), 418; https://doi.org/10.3390/ijms22010418 - 3 Jan 2021

Cited by 20 | Viewed by 3967

Abstract

Erectile Dysfunction (ED) is defined as the inability to maintain and/or achieve a satisfactory erection. This condition can be influenced by the presence of atherosclerosis, a systemic pathology of the vessels that also affects the cavernous arteries and which can cause an alteration of blood flow at penile level. Among the cardiovascular risk factors affecting the genesis of atherosclerosis, hyperhomocysteinemia (HHcys) plays a central role, which is associated with oxidative stress and endothelial dysfunction. This review focuses on the biological processes that lead to homocysteine-induced endothelial damage and discusses the consequences of HHcys on male sexual function Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

13 pages, 259 KiB

Open AccessReview

Seminal Plasma Proteomic Biomarkers of Oxidative Stress

by Rossella Cannarella, Andrea Crafa, Federica Barbagallo, Laura M. Mongioì, Rosita A. Condorelli, Antonio Aversa, Aldo E. Calogero and Sandro La Vignera

Int. J. Mol. Sci. 2020, 21(23), 9113; https://doi.org/10.3390/ijms21239113 - 30 Nov 2020

Cited by 31 | Viewed by 2987

Abstract

The prevalence of idiopathic male infertility is high, up to 75% of patients with abnormal sperm parameters. Hence, the research of its causes is mandatory. Oxidative stress (OS) can be responsible for male infertility in 30–80% of cases. In recent years, seminal plasma (SP) proteomics has developed as a useful tool to provide biomarkers of specific diseases. This systematic review aims to collect the available evidence on the changes of SP proteome in patients exposed to OS to provide possible SP biomarkers of sperm OS. To accomplish this, the following keyterms “seminal fluid proteome”, “seminal plasma proteome”, “oxidative stress”, and “sperm oxidative stress” were used and 137 records were found. Among these, 17 were finally included. Nine proteins involved with OS were found overexpressed in patients with OS. Twenty-three proteins were found differentially expressed in patients with clinical conditions associated with OS, such as varicocele, male accessory gland infection/inflammation, cigarette smoke, and obesity. These proteins do not seem to overlap among the clinical conditions taken into account. We speculate that specific SP proteins may mediate OS in different clinical conditions. Altogether, these results suggest that proteomics could help to better understand some of the molecular mechanisms involved in the pathogenesis of infertility. However, further studies are needed to identify potential biomarkers of male infertility with valuable clinical significance. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

14 pages, 1633 KiB

Open AccessReview

The Impact of Single- and Double-Strand DNA Breaks in Human Spermatozoa on Assisted Reproduction

by Ashok Agarwal, Cătălina Barbăroșie, Rafael Ambar and Renata Finelli

Int. J. Mol. Sci. 2020, 21(11), 3882; https://doi.org/10.3390/ijms21113882 - 29 May 2020

Cited by 55 | Viewed by 5195

Abstract

Several cellular insults can result in sperm DNA fragmentation either on one or both DNA strands. Oxidative damage, premature interruption of the apoptotic process and defects in DNA compaction during spermatogenesis are the main mechanisms that cause DNA breaks in sperm. The two-tailed Comet assay is the only technique that can differentiate single- (SSBs) from double- (DSBs) strand DNA breaks. Increased levels of the phosphorylated isoform of the H2AX histone are directly correlated with DSBs and proposed as a molecular biomarker of DSBs. We have carried out a narrative review on the etiologies associated with SSBs and DSBs in sperm DNA, their association with reproductive outcomes and the mechanisms involved in their repair. Evidence suggests a stronger negative impact of DSBs on reproductive outcomes (fertilization, implantation, miscarriage, pregnancy, and live birth rates) than SSBs, which can be partially overcome by using intracytoplasmic sperm injection (ICSI). In sperm, SSBs are irreversible, whereas DSBs can be repaired by homologous recombination, non-homologous end joining (NHEJ) and alternative NHEJ pathways. Although few studies have been published, further research is warranted to provide a better understanding of the differential effects of sperm SSBs and DSBs on reproductive outcomes as well as the prognostic relevance of DNA breaks discrimination in clinical practice. Full article

(This article belongs to the Special Issue Oxidative Stress in Metabolic and Endocrine Diseases: Basic and Translational Aspects)

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