Studies of the effects of Helminthosporium maydis race T toxin on mitochondria isolated from Texas male-sterile cytoplasm (cms-T) and nonsterile cytoplasm (N) corn have been conducted. Toxin added to cms-T mitochondria caused an energy-independent swelling in several media containing different osmoticants. Electron micrographs indicated that the swelling was caused by a specific disruption and vesiculation of the inner mitochondrial membrane. Toxin-induced swelling was correlated with an increase in the rate of NADH oxidation and a decrease in the rate of malate + pyruvate oxidation. We suggest that the toxin is not acting as a specific ionophoric agent or uncoupler but rather is causing a change in rate of substrate oxidation simply as a consequence of membrane disruption. We cannot definitely determine, however, whether changes in electron transport rates are due to interaction of the toxin with specific carriers in the mitochondrial electron transport pathways or whether the change in membrane configuration has altered the accessibility of various substrates to their oxidation sites.Mitochondria from four different N genotypes were unaffected by toxin. Mitochondria from five cms-T genotypes were all disrupted by the toxin, but each to a different extent. There was a correlation between the response of cms-T mitochondria to toxin and their field susceptibility to H. maydis within cms-T genotypes.