Nitrite and Nitric Oxide in Life

Topic Information

Dear Colleagues, 

In the process of biological evolution following oxygenic phototrophy, molecular oxygen has become the main electron acceptor during energy generation in the mitochondria of aerobic organisms on Earth. However, higher organisms have a backup system that uses nitrite as the electron acceptor for the generation of adenosine triphosphate and releases nitric oxide (NO). The release of NO dilates vessels and reduces mitochondrial oxygen consumption in ischemic tissues. There is evidence indicating that nitrite is the storage form of NO produced via canonical (NO synthase-mediated) and/or non-canonical (enterosalivary nitrate/nitrite NO) pathways and provides NO signaling under acidic, hypoxic, or physiological (e.g., gastric acidity and exercise) conditions in both cyclic guanosine monophosphate-dependent and -independent pathways. The local and systemic bioavailability of NO in the body may be closely involved in various physiological and pathological processes, including cardiovascular, musculoskeletal, neurotransmission, gastrointestinal, and host defense systems. In this regard, this Topic allows authors from different research areas to unite around one theme “Nitrite and Nitric Oxide in Life”, describe multidisciplinary applications, and develop new ideas. These collaborations could lead to the elucidation of the role of NO and nitrite in physiology and pathology for health promotion and the development of disease treatment. Therefore, we cordially invite authors to contribute original research articles and reviews that focus on this topic.

Prof. Dr. Jun Kobayashi
Dr. Kazuo Ohtake
Dr. Kunihiro Sonoda
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biology biology	3.6	5.7	2012	16.1 Days	CHF 2700
Biomedicines biomedicines	3.9	5.2	2013	15.3 Days	CHF 2600
Current Issues in Molecular Biology cimb	2.8	2.9	1999	16.8 Days	CHF 2200
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900
Journal of Molecular Pathology jmp	-	-	2020	25.4 Days	CHF 1000
Life life	3.2	4.3	2011	18 Days	CHF 2600

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Published Papers (5 papers)

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17 pages, 3777 KiB  

Open AccessArticle

An Evaluation of the Anti-Inflammatory Effects of a Thai Traditional Polyherbal Recipe TPDM6315 in LPS-Induced RAW264.7 Macrophages and TNF-α-Induced 3T3-L1 Adipocytes

by Phetpawi Subin, Pattraporn Sabuhom, Alisa Naladta, Prathan Luecha, Somsak Nualkaew and Natsajee Nualkaew

Curr. Issues Mol. Biol. 2023, 45(6), 4891-4907; https://doi.org/10.3390/cimb45060311 - 5 Jun 2023

Cited by 3 | Viewed by 2357

Abstract

TPDM6315 is an antipyretic Thai herbal recipe that contains several herbs with anti-inflammatory and anti-obesity activities. This study aimed to investigate the anti-inflammatory effects of TPDM6315 extracts in lipopolysaccharide (LPS)-induced RAW264.7 macrophages and TNF-α-induced 3T3-L1 adipocytes, and the effects of TPDM6315 extracts on [...] Read more.

TPDM6315 is an antipyretic Thai herbal recipe that contains several herbs with anti-inflammatory and anti-obesity activities. This study aimed to investigate the anti-inflammatory effects of TPDM6315 extracts in lipopolysaccharide (LPS)-induced RAW264.7 macrophages and TNF-α-induced 3T3-L1 adipocytes, and the effects of TPDM6315 extracts on lipid accumulation in 3T3-L1 adipocytes. The results showed that the TPDM6315 extracts reduced the nitric oxide production and downregulated the iNOS, IL-6, PGE₂, and TNF-α genes regulating fever in LPS-stimulated RAW264.7 macrophages. The treatment of 3T3-L1 pre-adipocytes with TPDM6315 extracts during a differentiation to the adipocytes resulted in the decreasing of the cellular lipid accumulation in adipocytes. The ethanolic extract (10 µg/mL) increased the mRNA level of adiponectin (the anti-inflammatory adipokine) and upregulated the PPAR-γ in the TNF-α induced adipocytes. These findings provide evidence-based support for the traditional use of TPDM6315 as an anti-pyretic for fever originating from inflammation. The anti-obesity and anti-inflammatory actions of TPDM6315 in TNF-α induced adipocytes suggest that this herbal recipe could be useful for the treatment of metabolic syndrome disorders caused by obesity. Further investigations into the modes of action of TPDM6315 are needed for developing health products to prevent or regulate disorders resulting from inflammation. Full article

(This article belongs to the Topic Nitrite and Nitric Oxide in Life)

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15 pages, 2330 KiB  

Open AccessArticle

Nitric Oxide Affects Heme Oxygenase-1, Hepcidin, and Transferrin Receptor Expression in the Placenta

by Patricia Principe, George T. Mukosera, Nikia Gray-Hutto, Ashra Tugung, Ciprian P. Gheorghe and Arlin B. Blood

Int. J. Mol. Sci. 2023, 24(6), 5887; https://doi.org/10.3390/ijms24065887 - 20 Mar 2023

Viewed by 2030

Abstract

Nitric oxide (NO) is a gasotransmitter that avidly binds both free and heme-bound iron, forming relatively stable iron nitrosyl compounds (FeNOs). We have previously demonstrated that FeNOs are present in the human placenta and are elevated in preeclampsia and intrauterine growth restriction. The [...] Read more.

Nitric oxide (NO) is a gasotransmitter that avidly binds both free and heme-bound iron, forming relatively stable iron nitrosyl compounds (FeNOs). We have previously demonstrated that FeNOs are present in the human placenta and are elevated in preeclampsia and intrauterine growth restriction. The ability of NO to sequester iron raises the possibility of the NO-mediated disruption of iron homeostasis in the placenta. In this work, we tested whether exposure of placental syncytiotrophoblasts or villous tissue explants to sub-cytotoxic concentrations of NO would elicit the formation of FeNOs. Furthermore, we measured changes in the mRNA and protein expression levels of key iron regulatory genes in response to NO exposure. Ozone-based chemiluminescence was used to measure concentrations of NO and its metabolites. Our results showed a significant increase in FeNO levels in placental cells and explants treated with NO (p < 0.0001). The mRNA and protein levels of HO-1 were significantly increased in both cultured syncytiotrophoblasts and villous tissue explants (p < 0.01), and the mRNA levels of hepcidin and transferrin receptor were significantly increased in culture syncytiotrophoblasts and villous tissue explants, respectively, (p < 0.01), while no changes were seen in the expression levels of divalent metal transporter-1 or ferroportin. These results suggest a potential role for NO in iron homeostasis in the human placenta and could be relevant for disorders of pregnancy such as fetal growth restriction and preeclampsia. Full article

(This article belongs to the Topic Nitrite and Nitric Oxide in Life)

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12 pages, 3071 KiB  

Open AccessArticle

Isodorsmanin A Prevents Inflammatory Response in LPS-Stimulated Macrophages by Inhibiting the JNK and NF-κB Signaling Pathways

by You Chul Chung, Ami Lee, Jin Ah Ryuk and Youn-Hwan Hwang

Curr. Issues Mol. Biol. 2023, 45(2), 1601-1612; https://doi.org/10.3390/cimb45020103 - 13 Feb 2023

Cited by 3 | Viewed by 1741

Abstract

Natural and synthetic chalcones exhibit anti-inflammatory, antitumoral, antibacterial, antifungal, antimalarial, and antitubercular activities. Isodorsmanin A (IDA), a chalcone, is a well-known constituent of the dried seeds of Psoralea corylifolia L. (PC). Although other constituents of PC have been widely investigated, there are no [...] Read more.

Natural and synthetic chalcones exhibit anti-inflammatory, antitumoral, antibacterial, antifungal, antimalarial, and antitubercular activities. Isodorsmanin A (IDA), a chalcone, is a well-known constituent of the dried seeds of Psoralea corylifolia L. (PC). Although other constituents of PC have been widely investigated, there are no studies on the biological properties of IDA. In this study, we focused on the anti-inflammatory effects of IDA and evaluated its effects on lipopolysaccharide (LPS)-stimulated macrophages. The results showed that IDA suppressed the production of inflammatory mediators (nitric oxide [NO] and prostaglandin E₂ [PGE₂]) and proinflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and interleukin-1β [IL-1β]) without cytotoxicity. In addition, it downregulated the mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) within the treatment concentrations. In our mechanistic studies, IDA inhibited the phosphorylation of the c-Jun N-terminal kinase (JNK), mitogen-activated protein kinase (MAPK), and protected the nuclear factor of the kappa light polypeptide gene enhancer in the B-cells’ inhibitor, alpha (IκB-α), from degradation, thus preventing the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells’ (NF-κB) transcription factor. Our results suggest that IDA is a promising compound for attenuating excessive inflammatory responses. Full article

(This article belongs to the Topic Nitrite and Nitric Oxide in Life)

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17 pages, 3112 KiB  

Open AccessArticle

Uric Acid Deteriorates Load-Free Cell Shortening of Cultured Adult Rat Ventricular Cardiomyocytes via Stimulation of Arginine Turnover

by Martin Weber, Rolf Schreckenberg and Klaus-Dieter Schlüter

Biology 2023, 12(1), 4; https://doi.org/10.3390/biology12010004 - 20 Dec 2022

Cited by 4 | Viewed by 1952

Abstract

Hyperuricemia is a risk factor for heart disease. Cardiomyocytes produce uric acid via xanthine oxidase. The enzymatic reaction leads to oxidative stress in uric-acid-producing cells. However, extracellular uric acid is the largest scavenger of reactive oxygen species, specifically to nitrosative stress, which can [...] Read more.

Hyperuricemia is a risk factor for heart disease. Cardiomyocytes produce uric acid via xanthine oxidase. The enzymatic reaction leads to oxidative stress in uric-acid-producing cells. However, extracellular uric acid is the largest scavenger of reactive oxygen species, specifically to nitrosative stress, which can directly affect cells. Here, the effect of plasma-relevant concentrations of uric acid on adult rat ventricular cardiomyocytes is analyzed. A concentration- and time-dependent reduction of load-free cell shortening is found. This is accompanied by an increased protein expression of ornithine decarboxylase, the rate-limiting enzyme of the polyamine metabolism, suggesting a higher arginine turnover. Subsequently, the effect of uric acid was attenuated if other arginine consumers, such as nitric oxide synthase, are blocked or arginine is added. In the presence of uric acid, calcium transients are increased in cardiomyocytes irrespective of the reduced cell shortening, indicating calcium desensitization. Supplementation of extracellular calcium or stimulation of intracellular calcium release by β-adrenergic receptor stimulation attenuates the uric-acid-dependent effect. The effects of uric acid are attenuated in the presence of a protein kinase C inhibitor, suggesting that the PKC-dependent phosphorylation of troponin triggers the desensitizing effect. In conclusion, high levels of uric acid stress cardiomyocytes by accelerating the arginine metabolism via the upregulation of ornithine decarboxylase. Full article

(This article belongs to the Topic Nitrite and Nitric Oxide in Life)

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13 pages, 990 KiB  

Open AccessArticle

TRPA1 Polymorphisms Modify the Hypotensive Responses to Propofol with No Change in Nitrite or Nitrate Levels

by Isabela Borges de Melo, Gustavo H. Oliveira-Paula, Letícia Perticarrara Ferezin, Graziele C. Ferreira, Lucas C. Pinheiro, Jose E. Tanus-Santos, Luis V. Garcia, Riccardo Lacchini and Waynice N. Paula-Garcia

Curr. Issues Mol. Biol. 2022, 44(12), 6333-6345; https://doi.org/10.3390/cimb44120432 - 14 Dec 2022

Viewed by 1823

Abstract

Anesthesia with propofol is frequently associated with hypotension. The TRPA1 gene contributes to the vasodilator effect of propofol. Hypotension is crucial for anesthesiologists because it is deleterious in the perioperative period. We tested whether the TRPA1 gene polymorphisms or haplotypes interfere with the [...] Read more.

Anesthesia with propofol is frequently associated with hypotension. The TRPA1 gene contributes to the vasodilator effect of propofol. Hypotension is crucial for anesthesiologists because it is deleterious in the perioperative period. We tested whether the TRPA1 gene polymorphisms or haplotypes interfere with the hypotensive responses to propofol. PCR-determined genotypes and haplotype frequencies were estimated. Nitrite, nitrates, and NOx levels were measured. Propofol induced a more expressive lowering of the blood pressure (BP) without changing nitrite or nitrate levels in patients carrying CG+GG genotypes for the rs16937976 TRPA1 polymorphism and AG+AA genotypes for the rs13218757 TRPA1 polymorphism. The CGA haplotype presented the most remarkable drop in BP. Heart rate values were not impacted. The present exploratory analysis suggests that TRPA1 genotypes and haplotypes influence the hypotensive responses to propofol. The mechanisms involved are probably other than those related to NO bioavailability. With better genetic knowledge, planning anesthesia with fewer side effects may be possible. Full article

(This article belongs to the Topic Nitrite and Nitric Oxide in Life)

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