부산대학교 도서관

Oral zinc supplementation corrects zinc deficiency and promotes good health. However, reports on zinc toxicity induced by excessive zinc ingestion remain limited. The aim of the present study was, therefore, to elucidate the effects of zinc excess on anemia. Over a 6-week period, one group of Sprague–Dawley rats was fed a standard diet containing 0.005% (w/w) zinc, whereas two other groups were fed a zinc excess diet including 0.2% (w/w) zinc, in which one group was intraperitoneally administered 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (tempol), a superoxide radical scavenger, for the final 8 days of the dietary duration. Blood samples were obtained and anemia-related parameters and oxidative stress markers were analyzed. An increase in red blood cell (RBC) osmotic fragility was observed, accompanied by microcytic hypochromic anemia, in the zinc excess group, which was restored to the standard group levels by tempol treatment. Additionally, a decrease in copper/zinc-superoxide dismutase (Cu/Zn-SOD) activity, a superoxide radical scavenger, was observed in the zinc excess groups, with an increase in the oxidative stress marker, 8-hydroxy-2'-deoxyguanosine, in the tempol-untreated zinc excess group. The relationship between the intestinal absorption rates of zinc and those of copper and iron was reciprocal. Thus, the microcytic hypochromic anemia may be, in part, owing to iron deficiency associated with zinc overload, whereas the increase in RBC osmotic fragility may be owing to oxidative stress derived from reduced Cu/Zn-SOD activity caused by copper deficiency associated with zinc overload.