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• W2534607545 abstract "Respiration utilizing NAD-linked substrates in mitochondria isolated from cotyledons of etiolated peas (Pisum sativum L. var. Homesteader) by sucrose density gradient centrifugation exhibited resistance to rotenone. The inhibited rate of a-ketoglutarate oxidation was equivalent to the recovered rate of malate oxidation. (The recovered rate is the rate following the transient inhibition by rotenone.) The inhibitory effect of rotenone on malate oxidation increased with increasing respiratory control ratios as the mitochondria developed. The cyanide-resistant and rotenone-resistant pathways followed different courses of development as cotyledons aged. The rotenone-resistant pathway transferred reducing equivalents to the cyanide-sensitive pathway. Malic enzyme was found to be inhibited competitively with respect to NAD by rotenone concentrations as low as 1.67 micromolar. In pea cotyledon mitochondria, rotenone was transformed into elliptone. This reduced its inhibitory effect on intact mitochondria. Malate dehydrogenase was not affected by rotenone or elliptone. However, elliptone inhibited malic enzyme to the same extent that rotenone did when NAD was the cofactor. The products of malate oxidation reflected the interaction between malic enzyme and malate dehydrogenase. Rotenone also inhibited the NADH dehydrogenase associated with malate dehydrogenase. Thus, rotenone seemed to exert its inhibitory effect on two enzymes of the electron transport chain of pea cotyledon mitochondria. Many different ideas have emerged to explain the ability of plant mitochondria to continue to respire in the presence of rotenone. These have not been totally substantiated and, in fact, many have been refuted. Some of the problems may arise from methodology used in investigations of the rotenone-resistant pathway. Palmer (18) questions the biochemical benefit to be derived from density gradient purification of mitochondria, and many workers have used mitochondria prepared by simple differential centrifugation in their studies of rotenone resistance. The validity of this procedure for such studies is investigated in this paper. Another practice that could lead to erroneous results is the seemingly indiscriminate use of inhibitors and cofactors to activate and stimulate the rotenone-resistant pathway. The present investigation was done using only rotenone as the activator of the pathway. Aspects of this study included the relationship of the rotenoneresistant pathway to the cyanide-resistant pathway, substrate and cofactor effects, and the mechanism for deactivation of rotenone. The enzymes for the oxidation of malate were also studied. On the basis of these results, a possible explanation for the control and operation of the rotenone-resistant pathway was developed." @default.
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• W2534607545 date "1981-01-01" @default.
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• W2534607545 title "The Effect of Rotenone on Respiration in Pea Cotyledon" @default.
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