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Abstract
Mitochondria isolated from control and irradiated (5000 Gy) bean hypocotyl segments oxidized both succinate and reduced nicotinamide adenine phosphate (NADPH). Results showed that control mitochondria were coupled and structurally intact; those from irradiated tissues revealed uncoupling and structural disintegration. A low ADP:O ratio oxidizing NADPH and the insensitivity of the latter to electron transport inhibitors such as retenone and antimycin A (aA) suggest an electron flow catalyzed by a distinct dehydrogenase which joins the main path at the III phosphorylation site. Enzymatic (NADPH + Fe 3+-induced) lipid peroxidation (LPO) was enhanced by radiation treatment by 34% above that of controls. A reduction in these values by superoxide dismutase (SOD), catalase and mannitol suggested participation of superoxide (O − 2), hydrogen peroxide (H 2O 2) and hydroxyl radical (OH) as the effective oxygen species initiating lipid peroxidation (LPO) in mitochondria. Protection against LPO by succinate in the absence or presence of malonate, rotenone and aA indicated NADPH-mediated LPO is controlled by electron transport-linked reduction of endogenous ubiquinone. A parallelism between O 2 consumption and lipid peroxidation values shows a direct relationship between the two processes. Antimycin A action is discussed in relation to a protonomotive Q-cycle mechanism.
Published Version
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