The present study was performed to evaluate the efficacy of
zinc treatment on colonic
antioxidant defense system and histoarchitecture in 1,2-dimethylhydrazine- (
DMH) induced colon
carcinogenesis in male Sprague-Dawley rats. The rats were segregated into four groups viz., normal control,
DMH treated,
zinc treated, DMH+zinc treated. Colon
carcinogenesis was induced through weekly
subcutaneous injections of
DMH (30 mg/kg
body weight) for 16 weeks.
Zinc (in the form of
zinc sulphate) was supplemented to rats at a dose level of 227 mg/L in
drinking water, ad libitum for the entire duration of the study. Increased
tumor incidence,
tumor size and number of
aberrant crypt foci (ACF) were accompanied by a decrease in lipid peroxidation,
glutathione-S-transferase,
superoxide dismutase (SOD) and
catalase. On the contrary, significantly increased levels of
reduced glutathione (GSH) and
glutathione reductase (GR) were observed in
DMH treated rats. Administration of
zinc to
DMH treated rats significantly decreased the
tumor incidence,
tumor size and
aberrant crypt foci number with simultaneous enhancement of lipid peroxidation, SOD,
catalase and
glutathione-S-transferase. Further, the levels of GSH and GR were also decreased following
zinc supplementation to
DMH treated rats. Well-differentiated signs of dysplasia were evident in colonic tissue sections by
DMH administration alone. However,
zinc treatment to
DMH treated rats greatly restored normalcy in the colonic histoarchitecture, with no apparent signs of
neoplasia. EDXRF studies revealed a significant decrease in tissue concentrations of
zinc in the colon following
DMH treatment, which upon
zinc supplementation were recovered to near normal levels. In conclusion, the results of this study suggest that
zinc has a positive beneficial effect against chemically induced colonic preneoplastic progression in rats induced by
DMH.