Inhibitory Effect of Thai Purple Rice Husk Extract on Chemically Induced Carcinogenesis in Rats.

This study investigated the cancer chemopreventive effects of an acidic methanol extract of purple rice husk on chemically induced carcinogenesis in rats. This purple rice husk extract (PRHE) had high polyphenol contents. Vanillic acid was a major phenolic compound in PRHE. Three major anthocyanins found in PRHE were malvidin-3-glucoside, peonidin-3-glucoside and cyanidin-3-glucoside. PRHE was not toxic and clastogenic in rats. The LD50 of PRHE was greater than 2000 mg kg-1 body weight (BW). The oral administration of 300 or 1000 mg kg-1 BW of PRHE for 28 days significantly decreased the number of micronucleated hepatocytes in diethylnitrosamine-initiated rats. The inhibitory mechanisms were associated with the reduction of cytochrome P450 2E1 expression and induction of some detoxifying enzymes in the liver. In addition, treatment with 500 mg kg-1 BW of PRHE for eight weeks did not induce preneoplastic lesions in the liver and colon. It significantly inhibited hepatic glutathione-S-transferase positive foci formation induced by diethylnitrosamine and 1,2-dimethylhydrazine by suppression of hepatocyte proliferation and induction of apoptosis. In conclusion, PRHE did not present toxicity, clastogenicity or carcinogenicity in rats. It exhibited cancer chemopreventive properties against chemically induced early stages rat hepatocarcinogenesis. Anthocyanins and vanillic acid might be candidate anticarcinogenic compounds in purple rice husk.

Anticlastogenicity and Anticarcinogenicity of Purple Rice Extract in Rats.

Oryza sativa L. var. indica cv. Kum Doi Saket is a pigmented rice variety grown in northern Thailand. Our previous study found that the methanol extract of purple rice seed had the highest level of antimutagenicity in a Salmonella mutation assay. The present study was designed to evaluate its in vivo anticlastogenic and anticarcinogenic potentials. The purple rice extract had no acute toxicity on rats. The oral administration of 1,000 mg/kg body weight (bw) of the extract for 28 days did not increase the number of micronucleated hepatocytes. Interestingly, it significantly reduced the amount of micronucleus formation in the liver of diethylnitrosamine (DEN)-treated rats. The inhibitory mechanism involved the induction of hepatic glutathione S-transferase (GST) activity. In addition, oral administration of 500 mg/kg bw extract for 10 weeks significantly decreased the number of hepatic GST placental form positive foci, but did not modulate the number of colonic aberrant crypt foci in DEN- and dimethylhydrazine-initiated rats. In conclusion, the methanol extract of purple rice seed showed no toxicity, clastogenicity, or carcinogenicity in laboratory rats. It did display chemopreventive activity against the early stages of rat hepatocarcinogenesis.