Abstract

Publisher Summary This chapter discusses the mitochondrial energy metabolism in chronic alcoholism. Long-term intake of large amounts of ethanol has deleterious effects on multiple organs in the body. It is associated with diseases of the liver, heart, skeletal muscle, pancreas, brain, and other tissues, and with compromised host defence mechanisms and tissue repair capacities. Almost all of the parameters that contribute to the control of mitochondrial energy conservation are affected when tissues are exposed acutely to ethanol and, depending on the tissue, changes in these components may occur in response to chronic ethanol intake. For instance, the oxidation of ethanol in the liver causes a marked change in the redox state of both cytosolic and mitochondrial NAD. This affects both the flux of electrons from other substrates, for example, fatty acids into the tricarboxylic acid cycle (TCA) cycle and the metabolite transfer processes associated with the shuttling of reducing equivalents from cytosolic NADH to the respiratory chain.

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