1. Control, vitamin E-deficient, vitamin E-supplemented (deficient with added ‘normal’ intake) and vitamin E-treated rats were given paracetamol at a dose of 25.5 mmol (4 g)/kg body weight. Control rats were also given paracetamol with or without simultaneous vitamin E.

2. Plasma aspartate aminotransferase and alanine aminotransferase activities increased to very high values (mean 2842 and 1241 i.u./l respectively) in the control group, and even higher (mean 8220 and 2320 i.u./l respectively) in the vitamin E-deficient group.

3. In the vitamin E-supplemented group the rises in activity were similar but rather less than in the control group (mean 2417 and 815 i.u./l) and in the vitamin E-treated group only very small rises (mean 177 and 98 i.u./l) were seen.

4. Histological evidence of hepatic necrosis correlated closely with plasma enzyme activities.

5. It appears that paracetamol-induced hepatic necrosis is potentiated in vitamin E deficiency and reduced by prior treatment with α-tocopherol.

6. Vitamin E administered simultaneously with paracetamol at 12.8 or 19.2 mmol/kg also greatly reduced the expected rise in serum enzyme activities.

7. These observations may shed some light on the mechanism of paracetamol-induced hepatic necrosis, and may form a basis for preventing or reducing this lesion in man.

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