Seppet E, Gruno M, Peetsalu A, Gizatullina Z, Nguyen HP, Vielhaber S, Wussling MH, Trumbeckaite S, Arandarcikaite O, Jerzembeck D, Sonnabend M, Jegorov K, Zierz S, Striggow F, Gellerich FN.
Abstract:
Mitochondrial dysfunction is a hallmark of almost all diseases. Acquired or inherited mutations of the mitochondrial genome DNA may give rise to mitochondrial diseases. Another class of disorders, in which mitochondrial impairments are initiated by extramitochondrial factors, includes neurodegenerative diseases and syndromes resulting from typical pathological processes, such as hypoxia/ischemia, inflammation, intoxications, and carcinogenesis.
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 and 45 min ischemia-damaged rat hearts.
