Abstract

Publisher Summary Respiratory decline, characteristic of vitamin $:-deficient liver tissue during the prenecrotic phase of dietary necrotic liver degeneration, consists of the breakdown of respiration in vitro , after brief, initial periods of normal oxygen consumption. The phenomenon is observed with liver slices and also homogenates, but not with isolated mitochondria from the livers of animals during the latent phase of the disease. Respiratory decline is not related to the rate of peroxide formation in the homogenate. Combination experiments disclosed that microsomes exert a deleterious effect on the respiring E-deficient mitochondria. This effect is prevented by complexing agents such as KDTA. The initiation of respiratory decline is related to disturbances of trace element balance. The initiation of respiratory decline is related to disturbances of trace element balance. A loss of titrable sulfhydryl groups is related to the breakdown of respiratory activity. Reduced glutathione and diniercaptopropanol prevent respiratory failure. It is concluded that the immediate cause of respiratory decline is a block, by a trace element(s), of sensitive sulfhydryl sites (or another highly sensitive site) on an enzyme indispensable for respiration in mitochondria.

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