65Zn kinetics as a biomarker of DMH induced colon carcinogenesis.

Dietary factors are considered crucial for the prevention of initiating events in the multistep progression of colon carcinoma. There is substantial evidence that zinc may play a pivotal role in host defense against several malignancies, including colon cancer. The present study was conducted to evaluate the kinetics of (65)Zn utilization following experimental colon carcinogenesis in rat model. Twenty rats were segregated into two groups viz., untreated control and dimethylhydrazine (DMH) treated. Colon carcinogenesis was established through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 16 weeks. Whole body (65)Zn kinetics followed two compartment kinetics, with Tb(1) representing the initial fast component of the biological half-life and Tb(2), the slower component. The present study revealed a significant depression in the Tb(1) and Tb(2) components of (65)Zn in DMH treated rats. Further, DMH treatment caused a significant increase in the percent uptake values of (65)Zn in the colon, small intestine, kidney and blood, whereas a significant decrease was observed in the liver. Subcellular distribution revealed a significant increase in (65)Zn uptake in the mitochondrial and microsomal fractions following 16 weeks of DMH supplementation. In conclusion, the present study demonstrated a slow mobilization of (65)Zn during promotion of experimentally induced colon carcinogenesis and provides a physiological basis for the role of (65)Zn in colon tumorigenesis, which may have clinical implications in the management of colon cancer.