Abstract
Experiments were performed with adrenalectomized, cortisol treated rats to examine the effect of CCl 4 intoxicated liver in metabolic studies, on the mechanism of hepatic steatosis. The results exclude any specificity of CCl 4 action. Using the model of liver tryptophan oxygenase induction after cortisol injection no reduction of protein biosynthesis and no disarrangement of endoplasmic reticulum could be seen without a concomitant decrease of the ATP/ADP ratio, glycogen storage and damage of mitochondrial structure, even if lowest doses were applied. On the other hand even lethal amounts of CCl 4 do not depress protein biosynthesis and ATP/ADP ratio below a relatively high minimal level. This may be caused by the fact that the dose dependent intoxication proceeds from the centre of the liver lobules to the periphery, as indicated by the histological study of stained glycogen granules. Thus CCl 4 intoxication appears to be an unspecific process, leading to the conclusion that CCl 4 poisoned liver should not be used as a model for studies on regulation of liver metabolism.
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