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Antioxidants
Special Issues
Oxidative Stress, Antioxidants and Gene Regulation
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Oxidative Stress, Antioxidants and Gene Regulation

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 18384

Special Issue Editors

Prof. Dr. Don-Kyu Kim

E-Mail Website
Guest Editor
Department of Integrative Food, Bioscience and Biotechnology, Chonnam National University, Gwangju, Republic of Korea
Interests: gene regulation; cell signaling; nuclear hormone receptor; transcription factor; transcriptional regulation; liver metabolism; metabolic disease
Special Issues, Collections and Topics in MDPI journals
Prof. Kamalakannan Radhakrishnan

E-Mail Website
Guest Editor
Cancer Mutation Reserch Center (CMRC), School of Medicine, Department of Cellular and Molecluar Medicine, Chosun University, Pilmun-daero, Korea
Interests: molecular mechanism of DNA damage repair (DDR) pathways; DNA repair; genome stability; oxidative-stress-induced DNA damage; role of antioxidants in DNA repair
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is typically defined as an imbalance between the production/accumulation of reactive oxygen species (ROS) and antioxidant defenses to remove these reactive products from the biological system. ROS are oxygen-derivatives with an uneven number of electrons, which causes unintentional reaction with other molecules in the system, potentially leading to a number of deleterious effects including DNA damage, aging and cancer. Several antioxidant compounds, like vitamin E, flavonoids and polyphenols, were exploited for their ability to neutralize these reactive products, and hence used to treat various pathological conditions ranging from inflammation to cancer. Cell signaling and gene regulation are the fundamental activities of the cell to control the transfer of genetic information from a gene to a protein throughout its life. Regulating the expression of various antioxidant genes at precise times by the biological system is exceedingly important to overcome the toxic effects of oxidative stress. Therefore, understanding the interaction between oxidative stress, antioxidants and gene regulation in physiological as well as in pathological conditions is essential for the prevention and treatment of oxidative-stress-related conditions. The scope of this Special Issue of Antioxidants shall cover a wide range of original and review articles aimed at exploring various aspects of oxidative stress, antioxidants and gene regulation in health and disease.

Prof. Don-Kyu Kim
Prof. Kamalakannan Radhakrishnan
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

  • oxidative stress
  • ROS
  • antioxidant system
  • cell signaling
  • gene regulation
  • transcriptional regulation
  • antioxidant gene expression
  • antioxidant therapy

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Published Papers (5 papers)

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Research

12 pages, 1940 KiB  
Article
Celastrol and Melatonin Modify SIRT1, SIRT6 and SIRT7 Gene Expression and Improve the Response of Human Granulosa-Lutein Cells to Oxidative Stress
by Rita Martín-Ramírez, Rebeca González-Fernández, Jairo Hernández, Pablo Martín-Vasallo, Angela Palumbo and Julio Ávila
Antioxidants 2021, 10(12), 1871; https://doi.org/10.3390/antiox10121871 - 24 Nov 2021
Cited by 13 | Viewed by 2315
Abstract
An excess of oxidative stress (OS) may affect several physiological processes fundamental to reproduction. SIRT1, SIRT6 and SIRT7 are involved in protection stress systems caused by OS, and they can be activated by antioxidants such as celastrol or melatonin. In this study, we [...] Read more.
An excess of oxidative stress (OS) may affect several physiological processes fundamental to reproduction. SIRT1, SIRT6 and SIRT7 are involved in protection stress systems caused by OS, and they can be activated by antioxidants such as celastrol or melatonin. In this study, we evaluate SIRT1, SIRT6 and SIRT7 gene expression in cultured human granulosa-lutein (hGL) cells in response to OS inductors (glucose or peroxynitrite) and/or antioxidants. Our results show that celastrol and melatonin improve cell survival in the presence and absence of OS inductors. In addition, melatonin induced SIRT1, SIRT6 and SIRT7 gene expression while celastrol only induced SIRT7 gene expression. This response was not altered by the addition of OS inductors. Our previous data for cultured hGL cells showed a dual role of celastrol as a free radical scavenger and as a protective agent by regulating gene expression. This study shows a direct effect of celastrol on SIRT7 gene expression. Melatonin may protect from OS in a receptor-mediated manner rather than as a scavenger. In conclusion, our results show increased hGL cells survival with melatonin or celastrol treatment under OS conditions, probably through the regulation of nuclear sirtuins’ gene expression. Full article
(This article belongs to the Special Issue Oxidative Stress, Antioxidants and Gene Regulation)
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15 pages, 2301 KiB  
Communication
Regulation of Heme Oxygenase and Its Cross-Talks with Apoptosis and Autophagy under Different Conditions in Drosophila
by Terence Al L. Abaquita, Milena Damulewicz, Debarati Bhattacharya and Elżbieta Pyza
Antioxidants 2021, 10(11), 1716; https://doi.org/10.3390/antiox10111716 - 28 Oct 2021
Cited by 6 | Viewed by 3109
Abstract
Heme oxygenase (HO) is one of the cytoprotective enzymes that can mitigate the effects of oxidative stress. Here, we found that the ho mRNA level oscillates in the brain of Drosophila melanogaster with two minima at the beginning of the day and night. [...] Read more.
Heme oxygenase (HO) is one of the cytoprotective enzymes that can mitigate the effects of oxidative stress. Here, we found that the ho mRNA level oscillates in the brain of Drosophila melanogaster with two minima at the beginning of the day and night. This rhythm was partly masked by light as its pattern changed in constant darkness (DD). It followed a similar trend in the clock mutant per01 under light/dark regime (LD12:12); however, differences between time points were not statistically significant. In older flies (20 days old), the rhythm was vanished; however, 15 days of curcumin feeding restored this rhythm with an elevated ho mRNA level at all time points studied. In addition, flies exposed to paraquat had higher ho expression in the brain, but only at a specific time of the day which can be a protective response of the brain against stress. These findings suggest that the expression of ho in the fly’s brain is regulated by the circadian clock, light, age, exposure to stress, and the presence of exogenous antioxidants. We also found that HO cross-talks with apoptosis and autophagy under different conditions. Induction of neuronal ho was accompanied by increased transcription of apoptosis and autophagy-related genes. However, this trend changed after exposure to curcumin and paraquat. Our results suggest that HO is involved in the control of apoptotic and autophagic key processes protecting the brain against oxidative damage. Full article
(This article belongs to the Special Issue Oxidative Stress, Antioxidants and Gene Regulation)
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15 pages, 3126 KiB  
Article
Epigallocatechin-3-Gallate Suppresses BMP-6-Mediated SMAD1/5/8 Transactivation of Hepcidin Gene by Inducing SMILE in Hepatocytes
by Yu-Ji Kim, Woo-Ram Park, Byungyoon Choi, Hueng-Sik Choi and Don-Kyu Kim
Antioxidants 2021, 10(10), 1590; https://doi.org/10.3390/antiox10101590 - 10 Oct 2021
Cited by 5 | Viewed by 2616
Abstract
Hepcidin, a major regulator of systemic iron homeostasis, is mainly induced in hepatocytes by activating bone morphogenetic protein 6 (BMP-6) signaling in response to changes in the iron status. Small heterodimer partner-interacting leucine zipper protein (SMILE), a polyphenol-inducible transcriptional co-repressor, regulates hepatic gluconeogenesis [...] Read more.
Hepcidin, a major regulator of systemic iron homeostasis, is mainly induced in hepatocytes by activating bone morphogenetic protein 6 (BMP-6) signaling in response to changes in the iron status. Small heterodimer partner-interacting leucine zipper protein (SMILE), a polyphenol-inducible transcriptional co-repressor, regulates hepatic gluconeogenesis and lipogenesis. Here, we examine the epigallocatechin-3-gallate (EGCG) effect on BMP-6-mediated SMAD1/5/8 transactivation of the hepcidin gene. EGCG treatment significantly decreased BMP-6-induced hepcidin gene expression and secretion in hepatocytes, which, in turn, abated ferroportin degradation. SMILE overexpression significantly decreased BMP receptor-induced hepcidin promoter activity. SMILE overexpression also significantly suppressed BMP-6-mediated induction of hepcidin mRNA and its secretion in HepG2 and AML12 cells. EGCG treatment inhibited BMP-6-mediated hepcidin gene expression and secretion, which were significantly reversed by SMILE knockdown in hepatocytes. Interestingly, SMILE physically interacted with SMAD1 in the nucleus and significantly blocked DNA binding of the SMAD complex to the BMP-response element on the hepcidin gene promoter. Taken together, these findings suggest that SMILE is a novel transcriptional repressor of BMP-6-mediated hepcidin gene expression, thus contributing to the control of iron homeostasis. Full article
(This article belongs to the Special Issue Oxidative Stress, Antioxidants and Gene Regulation)
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15 pages, 1737 KiB  
Article
Cystine and Methionine Deficiency Promotes Ferroptosis by Inducing B-Cell Translocation Gene 1
by Il-Je Cho, Doyeon Kim, Eun-Ok Kim, Kyung-Hwan Jegal, Jae-Kwang Kim, Sang-Mi Park, Rongjie Zhao, Sung-Hwan Ki, Sang-Chan Kim and Sae-Kwang Ku
Antioxidants 2021, 10(10), 1543; https://doi.org/10.3390/antiox10101543 - 28 Sep 2021
Cited by 11 | Viewed by 2829
Abstract
Ferroptosis is a type of programmed necrosis triggered by iron-dependent lipid peroxidation. We investigated the role of B-cell translocation gene 1 (BTG1) in cystine and methionine deficiency (CST/Met (−))-mediated cell death. CST/Met (−) depleted reduced and oxidized glutathione in hepatocyte-derived cells, increased prostaglandin-endoperoxide [...] Read more.
Ferroptosis is a type of programmed necrosis triggered by iron-dependent lipid peroxidation. We investigated the role of B-cell translocation gene 1 (BTG1) in cystine and methionine deficiency (CST/Met (−))-mediated cell death. CST/Met (−) depleted reduced and oxidized glutathione in hepatocyte-derived cells, increased prostaglandin-endoperoxide synthase 2 expression, and promoted reactive oxygen species accumulation and lipid peroxidation, as well as necrotic cell death. CST/Met (−)-mediated cell death and lipid peroxidation was specifically inhibited by pretreatment with ferroptosis inhibitors. In parallel with cell death, CST/Met (−) blocked global protein translation and increased the expression of genes associated with the integrated stress response. Moreover, CST/Met (−) significantly induced BTG1 expression. Using a BTG1 promoter-harboring reporter gene and siRNA, activating transcription factor 4 (ATF4) was identified as an essential transcription factor for CST/Met (−)-mediated BTG1 induction. Although knockout of BTG1 in human HAP1 cells did not affect the accumulation of reactive oxygen species induced by CST/Met (−), BTG1 knockout significantly decreased the induction of genes associated with the integrated stress response, and reduced lipid peroxidation and cell death in response to CST/Met (−). The results demonstrate that CST/Met (−) induces ferroptosis by activating ATF4-dependent BTG1 induction. Full article
(This article belongs to the Special Issue Oxidative Stress, Antioxidants and Gene Regulation)
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19 pages, 2798 KiB  
Article
N-Acetylcysteine Reduces the Pro-Oxidant and Inflammatory Responses during Pancreatitis and Pancreas Tumorigenesis
by Marie-Albane Minati, Maxime Libert, Hajar Dahou, Patrick Jacquemin and Mohamad Assi
Antioxidants 2021, 10(7), 1107; https://doi.org/10.3390/antiox10071107 - 11 Jul 2021
Cited by 5 | Viewed by 6041
Abstract
Pancreatitis, an inflammation of the pancreas, appears to be a main driver of pancreatic cancer when combined with Kras mutations. In this context, the exact redox mechanisms are not clearly elucidated. Herein, we treated mice expressing a KrasG12D mutation in pancreatic acinar [...] Read more.
Pancreatitis, an inflammation of the pancreas, appears to be a main driver of pancreatic cancer when combined with Kras mutations. In this context, the exact redox mechanisms are not clearly elucidated. Herein, we treated mice expressing a KrasG12D mutation in pancreatic acinar cells with cerulein to induce acute pancreatitis. In the presence of KrasG12D, pancreatitis triggered significantly greater redox unbalance and oxidative damages compared to control mice expressing wild-type Kras alleles. Further analyses identified the disruption in glutathione metabolism as the main redox event occurring during pancreatitis. Compared to the wild-type background, KrasG12D-bearing mice showed a greater responsiveness to treatment with a thiol-containing compound, N-acetylcysteine (NAC). Notably, NAC treatment increased the pancreatic glutathione pool, reduced systemic markers related to pancreatic and liver damages, limited the extent of pancreatic edema and fibrosis as well as reduced systemic and pancreatic oxidative damages. The protective effects of NAC were, at least, partly due to a decrease in the production of tumor necrosis factor-α (TNF-α) by acinar cells, which was concomitant with the inhibition of NF-κB(p65) nuclear translocation. Our data provide a rationale to use thiol-containing compounds as an adjuvant therapy to alleviate the severity of inflammation during pancreatitis and pancreatic tumorigenesis. Full article
(This article belongs to the Special Issue Oxidative Stress, Antioxidants and Gene Regulation)
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