Effect of toxins on T corn mitochondria: permeabilization

Since 1974 we have carried out experiments in order to point out the mechanism of the H. maydis, P. maydis toxins and methomyl in T corn mitochondria. These toxins are extracted from liquid cultures by G. Aranda et al. (Ann. Phytopathol. 10: 315, 1978). The methomyl from du Pont de Nemours is purified after recrystallization by Aranda. Since the rate of NADH oxidation is enhanced by H. maydis toxin, P. maydis toxin and methomyl, we look for which pathway the electron flow might follow: either the NADH external dehydrogenase or the NADH internal dehydrogenase. In the first case the stimulated rate of NADH oxidation must be inhibited by Antimycin A. In the second case the stimulated rate must be inhibited by both rotenon and Antimycin A.

Several facts conform to the second hypothesis: in the presence of rotenon the stimulated rate of NADH oxidation is not induced by the toxins or methomyl and the stimulated rate is inhibited by Antimycin A. Moreover the transport ability through the inner dehydrogenase complex is higher than through the outer membrane. The toxins or methomyl are able to induce a stimulating coefficient as high as 6 or 9 although the ADP cannot induce more than 3. Furthermore the toxins inhibit malate oxidation. We observed that malate oxidation can be restored by adding NAD. Nevertheless the phosphorylating ability is not restored by NAD.

In order to explain the toxin effect on T mitochondria both on the pathway of exogenous NADH oxidation and on malate oxidation we assume that the first effect of the inhibition is at the membrane level. Under the toxin action the membrane should be permeabilized so that the exogenous NADH could penetrate into the internal NADH dehydrogenase complex; on the other hand, the inner pool of the NAD should be diluted in the medium, consequently the malate dehydrogenase should be inhibited. In this way the first effect of the toxin should be to permeabilize the mitochondrial membranes. The leakage of NAD explains also the inhibition of the oxoglutarate. Further investigations may reveal a component involved in the loss of the ability to produce energy.

Michéle Paillard, Maryse Charbonnier and André Bervillé


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