Background: Ginger (Zingiber officinale Rosc) is a natural dietary component, which has antioxidant and anticarcinogenic properties. We investigated the effect of ginger on the initiation and post-initiation stages of 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Wistar rats.
Methods: Rats were given a weekly subcutaneous injection of DMH (20 mg/kg body weight) in the groin for 15 weeks. Ginger (50 mg/kg body weight/everyday p.o.) was given to the rats at the initiation, post-initiation stages of carcinogenesis. The activity of lipid peroxidation was studied by measuring the formation of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD), and the antioxidant status by measuring superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), glutathione reductase (GR), reduced glutathione (GSH), vitamins C, E, and A concentrations in the circulation of 1,2-dimethylhydrazine-induced experimental colon cancer.
Results: In the presence of a known colon carcinogen, DMH, plasma lipid peroxidation (TBARS, lipid hydroperoxides and conjugated dienes) and cancer incidence were significantly increased whereas enzymic (GPx, GST, GR, SOD and CAT) and non-enzymic antioxidant concentrations (GSH, vitamins C, E, and A) were decreased as compared to control rats. The number of tumors as well as the incidence of cancer was significantly decreased on treatment with ginger. In addition, ginger supplementation at the initiation stage and also at the post-initiation stages of carcinogenesis significantly reduced circulating lipid peroxidation and significantly enhanced the enzymic and non-enzymic antioxidants as compared to unsupplemented DMH-treated rats.
Conclusions: Ginger supplementation suppresses colon carcinogenesis in the presence of the procarcinogen DMH.