Acute Carbon Tetrachloride Hepatotoxicity

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Abstract
The general impression obtained from review of literature concerning CCI4-induced hepatotoxicity suggests that one should find a reciprocal relationship between serum enzymes and liver activity. This especially would apply if hepatocytes passively lost enzymes as a result of altered permeability or actual cellular disruption. Hepatocytes damaged by CCI4 may produce enzyme in response to injury. Whether such evolution could arise from de novo synthesis, activation of nascent enzyme, overloading of protein degradation pathways, or CCI4-induced steric rearrangements cannot be clearly determined. Regardless of the precise mechanism of enzymic elaboration, an increase in these cellular and serum catalysts could represent a homeostatic rather than retrograde response; GPT- and GOT-induced gluconeogenesis may be a compensatory response to glycogen depletion. Possible compensatory ends met by other cellular enzyme increases are not apparent al this lime.

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