LIPID PEROXIDATION AND ACTIVITIES OF ANTIOXIDANT ENZYMES IN IRON-DEFICIENCY AND EFFECT OF CARCINOGEN FEEDING

Iron deficiency has been implicated in increasing the risk of GI tract cancers in humans. Among various mechanisms of carcinogenesis, oxidat ive damage to DNA is well known and, hence, the present experimental s tudy was undertaken to investigate lipid peroxidation and activities o f different antioxidant enzymes in iron deficiency to explain the high er risk of tumorigenesis. Two groups of male weanling Fischer rats mai ntained on iron sufficient (C) or iron deficient (D) diets for a perio d of 32 weeks were subdivided, from 3 weeks onwards, into two subgroup s each. The carcinogen, dimethyl hydrazine was fed at a dose of 30 mg/ kg/week IG for a period of 9 weeks to groups that were designated as ( C+) and (D+). The other two subgroups (C-) and (D-) served as controls . After the experimental period, hepatic assays for lipid peroxidation (MDA production) and activities of various antioxidant enzymes were c arried out. The results showed that MDA production was elevated by 50% and activity of superoxide dismutase significantly depressed in carci nogen-fed, iron-deficient group (D+) by 28% compared to deficient (D-) group. There was an increase in hepatic selenium-dependent-glutathion e peroxidase activity in iron-deficient and iron-deficient, carcinogen -treated groups to the extent of 57 and 59%, respectively, as compared to controls; however, induction of enzyme in response to carcinogen f eeding, observed in the control group, was not evident in iron deficie ncy. Liver catalase was not altered between control and deficient grou ps. These results suggest that prolonged iron deficiency superimposed with carcinogen ingestion may render the host susceptible to a greater risk of tumorigenesis through oxidative stress.