ArticleRedox biology2016
The anthocyanin cyanidin-3-O-β-glucoside modulates murine glutathione homeostasis in a manner dependent on genetic background.
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 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
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- Effect of Purple Sweet Potato Using Different Cooking Methods on Cytoprotection against Ethanol-Induced Oxidative Damage through Nrf2 Activation in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Cyanidin-3-O-glucoside plays a protective role against renal ischemia/ reperfusion injury via the JAK/STAT pathway.Acta cirurgica brasileira · 2023Article
- Synergetic modulation of plant cadmium tolerance via MYB75-mediated ROS homeostasis and transcriptional regulation.Plant cell reports · 2022Article
- Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020Review
- Heritability of the aged glutathione phenotype is dependent on tissue of origin.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Suppression of Oxidative Stress and NFκB/MAPK Signaling by Lyophilized Black Raspberries for Esophageal Cancer Prevention in Rats.Nutrients · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anthocyanins are a class of phytochemicals that have generated considerable interest due to their reported health benefits. It has been proposed that commonly consumed anthocyanins, such as cyandin-3-O-β-glucoside (C3G), confer cellular protection by stimulating biosynthesis of glutathione (GSH), an endogenous antioxidant. Currently, it is unknown whether the health effects of dietary anthocyanins are genetically determined. We therefore tested the hypothesis that anthocyanin-induced alterations in GSH homeostasis vary by genetic background. Mice representing five genetically diverse inbred strains (A/J, 129S1/SvImJ, CAST/EiJ, C57BL/6J, and NOD/ShiLtJ) were assigned to a control or 100mg/kg C3G diet (n=5/diet/strain) for six weeks. GSH and GSSG levels were quantified in liver, kidney, heart, pancreas, and brain samples using HPLC. The C3G diet promoted an increase in renal GSH concentrations, hepatic GSH/GSSG, and cardiac GSH/GSSG in CAST/EiJ mice. C3G treatment also induced an increase in pancreatic GSH/GSSG in C57BL/6J mice. In contrast, C3G did not affect GSH homeostasis in NOD/ShiLtJ mice. Surprisingly, the C3G-diet caused a decrease in hepatic GSH/GSSG in A/J and 129S1/SvImJ mice compared to controls; C3G-treated 129S1/SvImJ mice also exhibited lower total glutathione in the heart. Overall, we discovered that C3G modulates the GSH system in a strain- and tissue-specific manner. To our knowledge, this study is the first to show that the redox effects of anthocyanins are determined by genetic background.
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