ArticleRedox biology2016
Epigallocatechin-3-gallate enhances key enzymatic activities of hepatic thioredoxin and glutathione systems in selenium-optimal mice but activates hepatic Nrf2 responses in selenium-deficient mice.
Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Enhanced bioavailability and short-term safety of a micellar green tea extract formulation co-delivered with N-acetylcysteine: a randomized crossover study in healthy adults.Frontiers in nutrition · 2026Trial
- Regular Consumption of Green Tea as an Element of Diet Therapy in Drug-Induced Liver Injury (DILI).Nutrients · 2024Review
- Disulfidptosis, A Novel Cell Death Pathway: Molecular Landscape and Therapeutic Implications.Aging and disease · 2024Review
- PSMD12 promotes non-small cell lung cancer progression through activating the Nrf2/TrxR1 pathway.Genes & genomics · 2024Article
- Oxidative Stress, Reductive Stress and Antioxidants in Vascular Pathogenesis and Aging.Antioxidants (Basel, Switzerland) · 2023Review
- (-)-Epigallocatechin-3-Gallate Attenuates the Adverse Reactions Triggered by Selenium Nanoparticles without Compromising Their Suppressing Effect on Peritoneal Carcinomatosis in Mice Bearing Hepatocarcinoma 22 Cells.Molecules (Basel, Switzerland) · 2023Article
- Potential of green tea EGCG in neutralizing SARS-CoV-2 Omicron variant with greater tropism toward the upper respiratory tract.Trends in food science & technology · 2023Review
- Therapeutic potential of green tea catechin, (-)-epigallocatechin-3-Phytomedicine plus : international journal of phytotherapy and phytopharmacology · 2023Review
- Antioxidant, antihyperglycemic, and antihyperlipidemic properties ofFrontiers in nutrition · 2023Article
- Dietary supplementation with biogenic selenium nanoparticles alleviate oxidative stress-induced intestinal barrier dysfunction.NPJ science of food · 2022Article
- Epigallocatechin Gallate Alleviates Down-Regulation of Thioredoxin in Ischemic Brain Damage and Glutamate-Exposed Neuron.Neurochemical research · 2021Article
- Potential protective mechanisms of green tea polyphenol EGCG against COVID-19.Trends in food science & technology · 2021Review
- Nutraceuticals in the Mediterranean Diet: Potential Avenues for Breast Cancer Treatment.Nutrients · 2021Review
- Physiological Dose of EGCG Attenuates the Health Defects of High Dose by Regulating MEMO-1 inOxidative medicine and cellular longevity · 2021Article
- Epigallocathechin-Frontiers in cellular and infection microbiology · 2021Article
- Epigallocatechin Gallate Slows Retinal Degeneration, Reduces Oxidative Damage, and Modifies Circadian Rhythms in P23H Rats.Antioxidants (Basel, Switzerland) · 2020Article
- Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes.Oxidative medicine and cellular longevity · 2020Article
- A mouse model of subacute liver failure with ascites induced by step-wise increased doses of (-)-epigallocatechin-3-gallate.Scientific reports · 2019Article
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Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenium participates in the antioxidant defense mainly through a class of selenoproteins, including thioredoxin reductase. Epigallocatechin-3-gallate (EGCG) is the most abundant and biologically active catechin in green tea. Depending upon the dose and biological systems, EGCG may function either as an antioxidant or as an inducer of antioxidant defense via its pro-oxidant action or other unidentified mechanisms. By manipulating the selenium status, the present study investigated the interactions of EGCG with antioxidant defense systems including the thioredoxin system comprising of thioredoxin and thioredoxin reductase, the glutathione system comprising of glutathione and glutathione reductase coupled with glutaredoxin, and the Nrf2 system. In selenium-optimal mice, EGCG increased hepatic activities of thioredoxin reductase, glutathione reductase and glutaredoxin. These effects of EGCG appeared to be not due to overt pro-oxidant action because melatonin, a powerful antioxidant, did not influence the increase. However, in selenium-deficient mice, with low basal levels of thioredoxin reductase 1, the same dose of EGCG did not elevate the above-mentioned enzymes; intriguingly EGCG in turn activated hepatic Nrf2 response, leading to increased heme oxygenase 1 and NAD(P)H:quinone oxidoreductase 1 protein levels and thioredoxin activity. Overall, the present work reveals that EGCG is a robust inducer of the Nrf2 system only in selenium-deficient conditions. Under normal physiological conditions, in selenium-optimal mice, thioredoxin and glutathione systems serve as the first line defense systems against the stress induced by high doses of EGCG, sparing the activation of the Nrf2 system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.