作者: Richard G. Hansford , Dmitry Zorov
DOI: 10.1007/978-1-4615-5653-4_23
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摘要: This paper reviews the model of control mitochondrial substrate oxidation by Ca2+ions. The mechanism is activation Ca2+ four dehydrogenases, viz. glycerol 3-phosphate dehydrogenase, pyruvate dehydrogenase multienzyme complex (PDH), NAD-linked isocitrate (NAD-IDH) and 2-oxoglutarate (OGDH). results in increase, or near-maintenance, NADH/NAD ratios activated state, depending upon tissue degree ‘downstream’ Ca2+, likely at level FIFo ATPase. Higher values redox span respiratory chain allow for greatly increased fluxes through oxidative phosphorylation with a minimal drop protonmotive force potential. As PDH, NAD-IDH OGDH are all located within inner membrane, it changes matrix free [Ca2+]m which act as signal to these activities. In this article, we review recent work measured cells tissues, using different techniques, special emphasis on question damping relative cytosol rapid transients e.g. cardiac myocytes. Further, put forward point view that failure energy transduction keep pace cellular needs some forms heart may involve be raised adequately dehydrogenases. We present new data show so myocytes isolated from animals suffering chronic, streptozocin-induced diabetes. raises possibility therapy based partial inhibition efflux pathways, thereby raising given, time-average value Ca2+. (Mol Cell Biochem 184: 359–369, 1997