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Antioxidants
Special Issues
Antioxidants and Omics Techniques
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Antioxidants and Omics Techniques

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 9276

Special Issue Editors

Prof. Dr. Zhongbing Lu

E-Mail Website
Guest Editor
College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Interests: cardiovascular disease; air pollution induced oxidative damage and metabolic diseases
Prof. Dr. Wenjun Ding

E-Mail Website
Guest Editor
College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Interests: environment and health; diabetes mellitus; obesity; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Liang-Jun Yan

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA
Interests: redox imbalance; oxidative stress; neuroprotection; diabetes; mitochondrial dysfunction; protein oxidation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Antioxidants are natural or artificial compounds that can scavenge free radicals and prevent oxidative damage. Diets rich in antioxidants have been found to be healthy. While both in vitro and in vivo studies have extensively demonstrated that antioxidant supplements are beneficial for oxidative stress-related disease and aging, the protective mechanistic pathways of antioxidants remain to be described. Such pathways must be defined prior to characterizing the prognosis and potential therapies and benefits presented by antioxidants to human health. Recently, omics techniques, such as genomics, transcriptomics, proteomics and metabolomics, have revolutionized biological and medical research. These new types of analysis allow a much deeper systematic insight into the protective mechanism of antioxidants and their interaction with genes or proteins.

This Special Issue aims to build a relationship between omics techniques and antioxidant therapy studies. Contributions to this Special Issue, both in the form of original research and review articles, may cover all aspects of omics techniques in order to deepen our understanding of the biological action of antioxidants. The following topics will be considered: uncovering the protective mechanism of antioxidants by transcriptomics or proteomics analysis; describing the metabolism of antioxidants and/or the interaction between antioxidants and endogenous metabolites; describing the effect of antioxidants on epigenetic modification/gut microbiota composition; and creating a database for the omics data of antioxidants.

Prof. Dr. Zhongbing Lu
Prof. Dr. Wenjun Ding
Dr. Liang-Jun Yan
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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
  • transcriptomics
  • proteomics and metabolomics
  • epigenetic modification
  • gut microbiota

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

13 pages, 3081 KiB  
Article
Inhibition of GCN2 Alleviates Cardiomyopathy in Type 2 Diabetic Mice via Attenuating Lipotoxicity and Oxidative Stress
by Juntao Yuan, Fang Li, Bingqing Cui, Junling Gao, Zhuoran Yu and Zhongbing Lu
Antioxidants 2022, 11(7), 1379; https://doi.org/10.3390/antiox11071379 - 16 Jul 2022
Cited by 4 | Viewed by 2948
Abstract
Diabetic cardiomyopathy (DCM) is a kind of heart disease that affects diabetic patients and is one of the primary causes of death. We previously demonstrated that deletion of the general control nonderepressible 2 (GCN2) kinase ameliorates cardiac dysfunction in diabetic mice. The aim [...] Read more.
Diabetic cardiomyopathy (DCM) is a kind of heart disease that affects diabetic patients and is one of the primary causes of death. We previously demonstrated that deletion of the general control nonderepressible 2 (GCN2) kinase ameliorates cardiac dysfunction in diabetic mice. The aim of this study was to investigate the protective effect of GCN2iB, a GCN2 inhibitor, in type 2 diabetic (T2D) mice induced by a high-fat diet (HFD) plus low-dose streptozotocin (STZ) treatments or deletion of the leptin receptor (db/db). GCN2iB (3 mg/kg/every other day) treatment for 6 weeks resulted in significant decreases in fasting blood glucose levels and body weight and increases in the left ventricular ejection fraction. GCN2iB treatment also attenuated myocardial fibrosis, lipid accumulation and oxidative stress in the hearts of T2D mice, which was associated with decreases in lipid metabolism-related genes and increases in antioxidative genes. Untargeted metabolomics and RNA sequencing analysis revealed that GCN2iB profoundly affected myocardial metabolomic profiles and gene expression profiles. In particular, GCN2iB increased myocardial phosphocreatine and taurine levels and upregulated genes involved in oxidative phosphorylation. In conclusion, the data provide evidence that GCN2iB effectively protects against cardiac dysfunction in T2D mice. Our findings suggest that GCN2iB might be a novel drug candidate for DCM therapy. Full article
(This article belongs to the Special Issue Antioxidants and Omics Techniques)
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12 pages, 2928 KiB  
Article
Melatonin Prevents NaAsO2-Induced Developmental Cardiotoxicity in Zebrafish through Regulating Oxidative Stress and Apoptosis
by Rui Yan, Jie Ding, Yuanjie Wei, Qianlei Yang, Xiaoyun Zhang, Hairu Huang, Zhuoyue Shi, Yue Feng, Heran Li, Hengdong Zhang, Wenjun Ding and Yan An
Antioxidants 2022, 11(7), 1301; https://doi.org/10.3390/antiox11071301 - 29 Jun 2022
Cited by 8 | Viewed by 2647
Abstract
Melatonin is an indoleamine hormone secreted by the pineal gland. It has antioxidation and anti-apoptosis effects and a clear protective effect against cardiovascular diseases. Our previous studies demonstrated that embryonic exposure to sodium arsenite (NaAsO2) can lead to an abnormal cardiac [...] Read more.
Melatonin is an indoleamine hormone secreted by the pineal gland. It has antioxidation and anti-apoptosis effects and a clear protective effect against cardiovascular diseases. Our previous studies demonstrated that embryonic exposure to sodium arsenite (NaAsO2) can lead to an abnormal cardiac development. The aim of this study was to determine whether melatonin could protect against NaAsO2-induced generation of reactive oxygen species (ROS), oxidative stress, apoptosis, and abnormal cardiac development in a zebrafish (Danio rerio) model. We found that melatonin decreased NaAsO2-induced zebrafish embryonic heart malformations and abnormal heart rates at a melatonin concentration as low as 10−9 mol/L. The NaAsO2-induced oxidative stress was counteracted by melatonin supplementation. Melatonin blunted the NaAsO2-induced overproduction of ROS, the upregulation of oxidative stress-related genes (sod2, cat, gpx, nrf2, ho-1), and the production of antioxidant enzymes (Total SOD, SOD1, SOD2, CAT). Melatonin attenuated the NaAsO2-induced oxidative damage, DNA damage, and apoptosis, based on malonaldehyde and 8-OHdG levels and apoptosis-related gene expression (caspase-3, bax, bcl-2), respectively. Melatonin also maintained the control levels of heart development-related genes (nkx2.5, sox9b) affected by NaAsO2. In conclusion, melatonin protected against NaAsO2-induced heart malformations by inhibiting the oxidative stress and apoptosis in zebrafish. Full article
(This article belongs to the Special Issue Antioxidants and Omics Techniques)
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18 pages, 3266 KiB  
Article
Vanadium(IV)-Chlorodipicolinate Protects against Hepatic Steatosis by Ameliorating Lipid Peroxidation, Endoplasmic Reticulum Stress, and Inflammation
by Yuanli Wang, Rulong Chen, Jingyi Li, Guodong Zeng, Juntao Yuan, Jingran Su, Chunyan Wu, Zhongbing Lu, Fang Zhang and Wenjun Ding
Antioxidants 2022, 11(6), 1093; https://doi.org/10.3390/antiox11061093 - 31 May 2022
Cited by 5 | Viewed by 2699
Abstract
Non-alcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. The aim of this study is to investigate the protective effects and the underlying mechanisms of vanadium(IV)-chlorodipicolinate ([VIVO(dipic-Cl)(H2O)2, [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. The aim of this study is to investigate the protective effects and the underlying mechanisms of vanadium(IV)-chlorodipicolinate ([VIVO(dipic-Cl)(H2O)2, VOdipic-Cl]) in a mouse model of NAFLD induced by a high-fat diet (HFD). VOdipic-Cl (10 mg/kg/day body weight) treatment for 4 weeks significantly controlled body weight gain, and effectively reduced the increase in serum and hepatic triglyceride (TG) and total cholesterol (TC) levels, mitigated pathological injury, decreased malondialdehyde (MDA) level, and inhibited endoplasmic reticulum (ER) stress and inflammatory response in the livers of C57BL/6 obese mice. Moreover, RNA-sequencing analysis revealed distinct transcriptional profiles with differentially expressed genes (DEGs) in livers. We found that VOdipic-Cl effectively down-regulated genes related to lipid synthesis and up-regulated genes related to fatty acid transport and lipolysis, and down-regulated the expression of genes related to ER stress and immune response in the livers of obese mice. In conclusion, VOdipic-Cl effectively prevented hepatic steatosis by controlling body weight, mitigating oxidative stress, and regulating the expression of genes related to lipid metabolism, ER stress and immune response, which provides new insights into the molecular mechanism of the protective effect of VOdipic-Cl against hepatic steatosis. Full article
(This article belongs to the Special Issue Antioxidants and Omics Techniques)
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