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Genetic Background Determines Anthocyanin Effects on Glutathione Redox Balance
Author(s) -
Norris Katie M,
Pazdro Robert
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.691.27
Subject(s) - glutathione , glutathione disulfide , chemistry , antioxidant , endogeny , biochemistry , redox , anthocyanin , medicine , endocrinology , biology , food science , enzyme , organic chemistry
Background Anthocyanins are secondary plant metabolites that provide the blue, red, and purple color of many plants. In recent years, these compounds have generated considerable interest among biomedical researchers 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 increasing biosynthesis of glutathione (GSH), an endogenous antioxidant. However, it is unclear whether anthocyanin‐induced health effects are subject to genetic control. In this project, we tested the hypothesis that genetic background regulates anthocyanin‐induced alterations in GSH levels and redox balance (GSH/GSSG). Methods Female mice representing five genetically diverse inbred strains (A/J, 129S1/SvImJ, CAST/EiJ, C57BL/6J, and NOD/ShiLtJ) were assigned to a control (n=5/strain) or 100 mg/kg C3G diet (n=5/strain) for six weeks. Liver, kidney, heart, pancreas, and brain were collected, and levels of GSH and GSSG were quantified by high‐performance liquid chromatography (HPLC). Total glutathione was calculated as GSH + 2GSSG, and redox balance was assessed by the GSH/GSSG ratio. Results C3G treatment increased GSH/GSSG in the livers (p = 0.041) and hearts (p = 0.028) of CAST/EiJ mice. C3G increased renal GSH levels (p = 0.01), increased total renal glutathione (p = 0.014), and decreased pancreatic GSSG levels (p = 0.021) in this strain as well. C3G‐treated C57BL/6J mice exhibited increased GSH/GSSG ratios in the pancreas (p = 0.042) only. NOD/ShiLtJ mice exhibited no differences between control and C3G treatment in any of the tissues, and no significant differences were found with C3G treatment in the brain in any of the five strains. Surprisingly, C3G negatively affected GSH levels in two strains. A/J mice fed a high C3G diet exhibited lower hepatic GSH concentrations (p = 0.044) and GSH/GSSG ratios (p = 0.017) compared to controls. 129S1/SvImJ mice also exhibited lower hepatic GSH/GSSG ratios (p = 0.007) with C3G treatment. In this strain, C3G also increased GSSG levels in the liver (p = 0.02) as well as decreased total glutathione in the heart (p = 0.034) compared to controls. Conclusions To our knowledge, this study is the first to show that the biological effects of anthocyanins are determined by genotype. This study also demonstrates that these effects occur in a tissue‐specific manner. Our data will inform future efforts to clarify genetic mechanisms that regulate differential responses to anthocyanin supplementation.