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QUERCETIN IMPACTS ETC/OXPHOS ACTIVITIES IN ISOLATED HEPATIC MITOCHONDRIA OF MICE
Author(s) -
Guo Xin,
Wu Lei,
Clarke Stephen,
Lin Dingbo
Publication year - 2015
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.29.1_supplement.607.21
Subject(s) - quercetin , mitochondrion , oxidative phosphorylation , mitochondrial biogenesis , oxidative stress , respiratory chain , chemistry , atp synthase , electron transport chain , biochemistry , biology , medicine , antioxidant , enzyme
Objective In general, quercetin attenuates oxidative stress and enhances mitochondrial biogenesis in the development of obesity and/or diabetes. In this study we wished to determine how quercetin impacted the mitochondrial function by examining mitochondrial electron transport chain/oxidative phosphorylation (ETC/OXPHOS) in isolated mouse hepatic mitochondria. Methods Male wild type 129 S6 (WT) mice, at 6 weeks of age, were used. Isolated hepatic mitochondria were treated with quercetin (0, 2.5, 5, 10, and/or 20 μM) for 15 min. Then the individual ETC complex activity, basal oxygen consumption, maximum ATP utilization, maximum respiratory capacity, and proton leak were measured via assays of electron flow and coupling. Results Quercetin decreased the basal respiratory rate and the maximum respiratory capacity. No change was observed in maximum ATP utilization, proton leak, and activities of ETC complex I, II and III. However, quercetin at a low dose (e.g., 2.5 μM) significantly increased the ETC complex IV activity. The effect was then diminished dose dependently. Conclusions Quercetin may lower the mitochondrial respiratory activity through mediating the ETC complex IV.