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Helminthosporium maydis Race T Toxin Induces Leakage of NAD⁺ from T Cytoplasm Corn Mitochondria ¹

^a Department of Plant Breeding and Biometry, Cornell University, Ithaca, New York 14853

The mechanism by which Helminthosporium maydis race T toxin inhibits respiration dependent on NAD⁺-linked substrates in T cytoplasm corn mitochondria was investigated. The toxin did not cause leakage of the soluble matrix enzyme malate dehydrogenase from the mitochondria or inhibit malate dehydrogenase or isocitrate dehydrogenase directly. The toxin did increase the permeability of the inner membranes of T cytoplasm, but not N cytoplasm, mitochondria to NAD⁺. Added NAD⁺ partially or fully restored toxin-inhibited electron transport in T cytoplasm mitochondria. Thiamin pyrophosphate had a similar effect when malate was the substrate. It was concluded that the inhibition of respiration of NAD⁺-linked substrates by the toxin is due to depletion of the intramitochondrial pool of NAD⁺ and other coenzymes.

¹ This work was supported by Rockefeller Foundation Grant 75002. D. E. M. was supported by a Rockefeller Foundation Postdoctoral Fellowship. Paper No. 687 in the Plant Breeding Series. Portions of this research were reviewed at the Second International Mycological Congress, 1977 (14).

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