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Anthocyanins as substrates for mitochondrial complex I – protective effect against heart ischemic injury
Author(s) -
Skemiene Kristina,
Liobikas Julius,
Borutaite Vilmante
Publication year - 2015
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.13195
Subject(s) - mitochondrion , ischemia , delphinidin , pelargonidin , coenzyme q – cytochrome c reductase , respiration , chemistry , cellular respiration , biochemistry , pharmacology , biology , medicine , cyanidin , antioxidant , anatomy , cytochrome c
Anthocyanins, a subclass of flavonoids, are known to protect against myocardial ischemia; however, little is known about their direct, acute effects on mitochondria injured by the ischemic insult. In this study, the effects of delphinidin 3‐ O ‐glucoside (Dp3G), cyanidin 3‐ O ‐glucoside (Cy3G) and pelargonidin 3‐ O ‐glucoside (Pg3G) on the activity of complex I of the mitochondrial respiratory chain were studied in mitochondria isolated from normal rat hearts and rat hearts subjected to ischemia for 45 min. Cy3G and Dp3G increased the activity of complex I, measured in the presence or absence of coenzyme Q 1 (CoQ 1 ), in ischemia‐damaged mitochondria, whereas in nonischemic mitochondria the effect was observed only in the absence of CoQ 1 . Dp3G and Cy3G but not Pg3G increased state 3 respiration and ATP synthesis with NADH ‐dependent substrates in mitochondria after ischemia. The results suggest that certain anthocyanins can act as electron acceptors at complex I, and bypass ischemia‐induced inhibition, resulting in increased ATP production after ischemia. This study provides new information on a possible role of certain anthocyanins in the regulation of energy metabolism in mammalian cells.

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