ABSTRACT
The mitochondrial organelle is an extremely efficient engine capable of enzymati cally oxidizing various fuel molecules (amino acids, fatty acids, and carbohy drates) and harnessing the energy released from these exergonic reactions. De spite the extraordinary efficiency of mitochondrial enzyme complexes in catalyzing the release of energy from respiratory substrates, inevitable side reac tions occur which result in a loss of efficiency and the release of oxidizing agents as side products. Since mitochondrial bioenergetics ultimately depends on the controlled four-electron reduction of oxygen to water, the side products most associated with mitochondrial inefficiency are the one-and two-electron reduc tion products of oxygen, superoxide ( 0 2~) and hydrogen peroxide (H20 2), respec tively. Both 0 2~ and H20 2 are reactive oxidizing agents capable of attacking and lesioning membranes, enzymes, and genomic components to the detriment of the cell and the organism. The approximate yield of 0 2" plus H20 2 (collectively referred to as reactive oxygen species, or ROS) is generally estimated at 1-2% of total mitochondrial oxygen consumption (1,2).
