Recent evidence suggests that mitochondrial complex II is an essential mediator of
myocardial ischemia-
reperfusion injury. The present study aimed to investigate the effects of
fatty acid supplementation or high-fat diet (HFD) on cardiac mitochondrial activity. The changes of complex I and complex II activities and mitochondrial oxygen consumption rate (OCR) following
hypoxia and re-oxygenation under these conditions were studied. Our results have shown that OCR (mitochondrial activity) was significantly increased with
palmitoylcarnitine supplementation in mitochondria-enriched fraction from C57BL/6 mice hearts. Mitochondrial complex I activity was unaffected by
palmitoylcarnitine but complex II activity was enhanced. Re-oxygenation following 30-min
hypoxia transiently increased OCR but such an effect on OCR was abolished by complex II inhibitor,
malonate, but not by complex I inhibitor,
rotenone, despite that complex I activity was significantly increased with re-oxygenation following
hypoxia in the presence of
palmitoylcarnitine. Furthermore, OCR and complex II activity were significantly increased in the mitochondria from high-fat diet mice heart compared with those of normal or
low-fat diet mice. Re-oxygenation to mitochondria following 30-min
hypoxia increased OCR in all three groups but significantly more in HFD.
Malonate abolished re-oxygenation-induced OCR increment in all groups. Our results indicate that complex II activity and OCR are enhanced with
palmitoylcarnitine or in HFD mice heart. Although re-oxygenation following
hypoxia enhanced complex II and complex I activities, complex II plays an important role in increasing mitochondrial activity, which may be instrumental in myocardial injury following ischemic reperfusion.