Diabetes mellitus is a metabolic disorder associated with increased formation of free radicals. The objective of our study was to determine whether ferulic acid (FA), a phenolic acid, has any role to play in diabetes induced free radical formation. Diabetes was induced with streptozotocin. The levels of blood glucose, thiobarbituric acid reactive substances (TBARS), hydroperoxides and free fatty acids (FFA) increased in the liver of diabetic animals. The activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) decreased in the liver. Histopathology of pancreas also shows shrunken islets. Supplementation of FA to the diabetic rats resulted in a decrease in the levels of glucose, TBARS, hydroperoxides, FFA and an increase in reduced glutathione (GSH). FA also resulted in increased activities of SOD, CAT, GPx and expansion of pancreatic islets. The effect was much pronounced with lower dose treatment. Thus our study shows that administration of ferulic acid helps in enhancing the antioxidant capacity of these diabetic animals by neutralizing the free radicals formed thereby reducing the intensity of diabetes.

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Prevention of cancer remains a primary need and new chemopreventive agents must be developed for this purpose. Towards this goal, a chemoprevention study was conducted to evaluate the activity of resveratrol (Res), a phytoalexin, as an inhibitor of colon carcinogenesis. Wistar male rats were divided into six groups, group 1 were control rats, group 2 were control rats that received Res (8 mg/kg body wt p.o. everyday), rats in groups 3-6 were treated weekly with 1,2-dimethylhydrazine (DMH, 20 mg/kg body wt, s.c. x 15 times). In addition, groups 4, 5 and 6 received Res as in group 2. Modifying effects were assessed using aberrant crypt foci (ACF) and the extent of histopathological lesions as end point markers. At the end of 30 weeks, Res markedly reduced tumor incidence, the degree of histological lesions and also the size of tumors significantly (P < 0.05) as compared with the rats treated with unsupplemented DMH. The number of ACF consisting of more than six aberrant crypts per rat was observed in group 6 (6.2 +/- 1.4), group 5 (7.7 +/- 1.0) and group 4 (8.2 +/- 1.4) which were significantly lower than that of group 3 (22.3 +/- 2.4) (P < 0.05). The most pronounced inhibition of ACF development was noted in rats fed Res for the entire period and also during the post-initiation period. Also, Res administration lowered the number of argyrophilic nucleolar organizing region-associated proteins (AgNORs) per nucleus in non-lesional colonic crypts, which reflects the cell proliferation activity. Oxidative imbalance in DMH-treatment was significantly (P < 0.01) modulated on Res supplementation as indicated by optimal concentration of thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH). The results of our study suggest Res to be an effective chemopreventive agent, which suppresses DMH-induced colon carcinogenesis at various stages.