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Modulation of colonic aberrant crypt foci and proliferative indexes in colon and prostate glands of rats by vitamin E

Yao, K., Latta, M., Bird, R.P.
Nutrition and cancer 1996 v.26 no.1 pp. 99-109
nutrient intake, carcinogenesis, rats, dose response, liver, antigens, acid phosphatase, experimental diets, disease prevention, vitamin E, body weight, intestinal mucosa, blood plasma, cell proliferation, alkaline phosphatase, colon
The effect of a high vitamin E diet on the early stages of colon carcinogenesis and on the proliferative indexes in the colon and in the prostate glands was investigated in rats. F344 male rats were injected with azoxymethane (AOM, 15 mg/kg sc). One week later, animals were randomly allocated into two dietary groups (n = 8 rats/group): normal vitamin E (50 IU/kg diet) and high vitamin E (200 IU/kg diet). The basal diet was the AIN-76 diet modified to contain high corn oil (23% wt/wt). After eight weeks of feeding, concentrations of vitamin E in plasma, liver, and prostate were analyzed. Enumeration of aberrant crypt foci (ACF) in colons and proliferative indexes of colons and prostate glands were determined. The total number of ACF and the average number of aberrant crypts (AC) per focus were similar in both dietary groups. ACF were classified as small (1-3 crypts/focus), medium (46 crypts/focus), or large (greater than or equal to 7 crypts/focus). Only the ACF in the small category showed a significant treatment effect, with values being lower in the high vitamin E group than in the control group (p less than or equal to 0.05). No significant difference was observed in colonic proliferative indexes assessed by enumeration of metaphase cells, S phase cells, or cells exhibiting proliferative cell nuclear antigen (PCNA). The PCNA labeling index in the prostate glands and the activity of prostatic acid phosphatase in plasma were higher in high vitamin E fed rats (p less than or equal to 0.05) than in control animals. The present study demonstrates that additional vitamin E does not inhibit the induction and growth of ACF; also it enhances the proliferative status of the prostate glands.