It has been confirmed that lipid peroxidation of liver homogenates is increased following acute ethanol intoxication. Studies with recombined fractions of the liver suggest that the cause for the ethanol‐induced increase in malonic dialdehyde production is located in the soluble fraction. Reduced glutathione content of the liver supernatant is decreased following ethanol intoxication. The decrement, however, occurs after the increase in malonic dialdehyde production takes place. Glutathione reductase and glutathione peroxidase activities of the liver are unaffected by ethanol administration. It is suggested that the decrease in reduced glutathione content may reflect a condition of increased peroxidation in vivo.
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Comporti et al. (1973) studied this question.
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