Mitochondrial Transhydrogenase: Yin and Yang of Antioxidative Capacity in Cardiac Myocytes

Abstract

depolarization of mitochondria may be altered by extracellular glucose. Oxidative phosphorylation requires the large aJmito and when the mitochondria are depolarized, oxidative phosphorylation becomes uncoupled and ATP production falls. Here we investigate the effect of hyperglycemia (30 mM versus the physiological glucose of 5 mM) on mitochondrial aJmito under photoninduced oxidative stress in rat ventricular myocytes. Using a buffered physiologic salt solution on quiescent ventricular myocytes, changing the [glucose] has dramatic effect on the rate of aJmito depolarization. The rate of depolarization was significantly decreased in the presence of high glucose (the time-to-50% depolarization was increased from 250 s to 500s). These results were carried out in the absence of insulin. We conclude that hyperglycemia appears to protect mitochondrial function in quiescent heart cells from photon-induced oxidative stress. It is not yet clear how this apparent protection may change as metabolic load and muscle work increases, nor is it clear whether the absence of fatty acid substrates will increase or decrease this seemingly protective effect.