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No inhibition of gamma-glutamyl transpeptidase-positive foci by vitamin E with or without phenobarbital

Lii, C.K., Ko, J.J., Chen, H.W.
Nutrition and cancer 1997 v.27 no.2 pp. 200-205
aminoacyltransferases, prostaglandins, nutrient-drug interactions, dose response, nitrosamines, glutathione transferase, phenobarbital, oxidation, females, phospholipids, weight, docosenoic acids, body weight, vitamin supplements, rats, enzyme activity, thiobarbituric acid-reactive substances, weight gain, liver, docosahexaenoic acid, eicosapentaenoic acid, experimental diets, vitamin E, arachidonic acid
The effect of vitamin E on -gamma-glutamyl transpeptidase-positive foci, with or without phenobarbital, was investigated. Groups of six female Sprague-Dawley rats were initiated with diethylnitrosamine (15 mg/kg) at 24 hours of age. After weaning, they were fed diets with 10% (wt/wt) fish oil; the diets contained 0, 5,000, or 15,000 ppm vitamin E supplementation with or without phenobarbital (500 ppm) for six months. Phenobarbital significantly increased liver weight and liver weight as a percentage of body weight (p < 0.05), suggesting a liver hypertrophic effect of phenobarbital. Phenobarbital significantly decreased hepatic phospholipid arachidonate, eicosapentaenoate, and docosahexaenoate (p <0.05); this may indicate that phenobarbital stimulates phospholipase A2 activity and results in the increased release of polyunsaturated fatty acids from phospholipids and the decrease of hepatic phospholipid polyunsaturated-to-saturated fat ratio. In rats fed phenobarbital, hepatic vitamin E content was lower than in rats fed no phenobarbital; this suggests that phenobarbital causes oxidative stress or induces enzymes that metabolize the vitamin. Phenobarbital exposure significantly increased hepatic prostaglandin F2alpha and glutathione S-transferase activity (p <0.05). Vitamin E did not influence hepatic gamma-glutamyl transpeptidase-positive foci area and number with or without phenobarbital, and phenobarbital showed a strong promoting action on enzyme-altered hepatic foci.