ZINC-DEFICIENCY, ERYTHROCYTE PRODUCTION, AND CHROMOSOMAL DAMAGE IN PREGNANT RATS AND THEIR FETUSES

During periods of rapid growth and development, chromosomal and DNA da mage has been observed in hepatic tissue samples of zinc-deprived anim als. In this study, the erythrocyte micronucleus assay was used to est imate cytogenetic damage due to zinc deprivation in pregnant rat dams and their fetuses. Rat dams were assigned to one of three dietary grou ps on day 0 of gestation: zinc deficient (<0.5 mu g of zinc/g of diet) , zinc adequate (50 mu g of zinc/g of diet), and pair-fed (50 mu g of zinc/g of diet in an amount matched to daily food intake of the zinc-d eficient group). By day Ip of gestation, the zinc-deprived darns had g ained no weight during pregnancy and had resorbed nearly half their im plantation sites. Of their remaining fetuses, one-third were malformed , and all were growth-retarded. Fetuses from the zinc-deficient group had only one-half of the liver zinc concentration of fetuses in the zi nc-adequate and pair-fed groups. In contra:Ft, zinc deprivation of the darns caused no change in liver zinc concentrations but reduced plasm a and bone zinc concentrations and elevated liver iron concentrations nearly 2 fold. In spite of their excessively high liver iron stores, e rythrocyte production, estimated from the ratio of newly formed to old er cells, was suppressed in the zinc-deprived darns. There was no obse rvable increase in the frequency of micronuclei, a measure of chromoso mal damage, in recently formed or mature erythrocytes in zinc-deficien t rat darns or their fetuses.