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Effect of diphtheria toxin fragment A on energy coupling in mitochondria. Studies on mouse liver mitoplasts
Authors:Abraham K Abraham  Torgeir Flatmark  Alexander Pihl  Anni Vedeler
Institution:1.Norsk Hydro’s Institute for Cancer Research,The Norwegian Cancer Society,Montebello,Norway;2.Department of Biochemistry,The University of Bergen,Arstadveien 19,Norway
Abstract:The effect of intact diphtheria toxin and of its fragment A on protein synthesis in mouse liver mitoplasts (digitonin-treated mitochondria) was studied. Fragment A inhibited protein synthesis in intact mitoplasts to the same extent as the uncoupler, carbonylcyanidep-trifluoromethoxyphenylhydrazone, but similar effects were not observed in lyzed mitoplasts. Intact diphtheria toxin was without effect in either case.Fragment A strongly stimulated mitochondrial ATPase activity. At concentrations which efficiently inhibited mitochondrial protein synthesis and stimulated ATPase activity, fragment A had no effect on the intramitochondrial concentration of nicotin-amide adenine dinucleotides. Moreover, it did not catalyze ADP ribosylation of mitochondrial proteins. The results indicate that the effects observed did not involve the NAD+-glycohydrolase activity of fragment A.125I]-Labelled fragment A was bound to mitoplasts to about the same extent as the labelled intact diphtheria toxin.The present results suggest that fragment A of diphtheria toxin is capable of inhibiting the energy coupling in mitoplasts, thereby inhibiting protein synthesis. The detailed mechanism of the uncoupling and its possible physiological significance remains to be elucidated
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