Effects of Thermal Treatment on Mitochondria of Brain, Liver and Ascites Cells

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Abstract
The oxidative phosphorylation and respiratory control of mouse brain, liver and Ehrlich ascites tumour cells have been studied after preincubating the mitochondria in vitro at temperatures up to 45o. Respiration, phosphorylation and respiratory control were measured with malate plus pyruvate or succinate as substrates. In addition antimycin‐sensitive ferricyanide reduction by succinate (with rotenone and KCN present) as well as ascorbate oxidation (with N, N, N’, N’,‐tetramethyl‐1.4‐phenylenediamine (TMPD), rotenone and antimycin present) and coupled phosphorylation were determined. The results indicate that electron transport in the succinate‐cytochrome c‐region is more heat‐sensitive than that of the cytochrome c‐oxygen region. Moreover, both this inhibition of electron transport, loss of respiratory control and uncoupling of phosphorylation are likely to be primary effects of heat treatment. Leakage of endogenous cytochrome c to the surrounding medium has been demonstrated, indicating membrane damage as an early effect of heat treatment. The investigated tissues show considerable variations in heat sensitivity of oxidative phosphorylation, brain mitochondria being the most heat resistant. Oxidative phosphorylation of mitochondria prepared from heat‐treated intact ascites cells is more heat resistant than that of in vitro heat‐treated mitochondria, as higher temperatures are required to produce similar effects.