THE EFFECT OF CHILLI INGESTION ON GASTROINTESTINAL MUCOSAL PROLIFERATION AND AZOXYMETHANE-INDUCED CANCER IN THE RAT

Of the three main races of Singapore, Malays and Indians are less susceptible to gastric and colorectal carcinoma and peptic ulcer when compared with Chinese. Racial differences in dietary habits include a smaller amount of chilli consumed by the Chinese when compared with the other two races. Chilli may be expected to accelerate gastrointestinal transit and hence to inhibit colonic carcinogenesis, while its active ingredient capsaicin protects against experimental gastric mucosal injury. The effect of chilli consumption was studied in relation to: (i) gastrointestinal crypt cell production rate and nucleic acid content as indices of mucosal proliferation, which is related to the risk of development of gastrointestinal cancer and peptic ulcer; and (ii) azoxymethane-induced intestinal cancer. Sprague-Dawley rats (n = 102) received either standard powdered chow or chow supplemented with 100 or 200 mg of chilli powder daily for 1, 18 or 24 weeks. Gastric, small-bowel and colonic crypt cell production rates were studied at all three time periods, while mucosal DNA, RNA and protein contents were measured at 1 and 24 weeks. While crypt cell production rates were unaffected by chilli ingestion, mucosal contents of nucleic acid and protein were mostly increased in chilli-fed animals compared to controls, especially in the colon at 24 weeks. A further 99 rats received subcutaneous injections of either azoxymethane 15 mg/kg/week x 6 or sterile water and were randomized to the same three dietary groups for 26 weeks. The number, size and location of benign and malignant duodenal and colonic tumours were unaffected by chilli intake. Chilli therefore had no effect on mucosal proliferation, although a moderate effect on mucosal mass was seen. It did not alter intestinal carcinogenesis.