Severe zinc deficiency in rodent models has been shown to influence the frequency of single-strand breaks in DNA isolated from liver. In the current study, we investigated whether DNA isolated from infant monkeys born to mothers fed zinc-restricted diets would be characterized by higher than normal levels of DNA damage. DNA was isolated from 30-day-old infants born to dams fed low zinc (2 or 4 micrograms Zn/g) or control zinc (50 micrograms Zn/g) diets. The amount of single-strand breaks in liver DNA was significantly higher in the low zinc group than in controls; consistent with the above, there was a trend for higher steady state levels of liver 8-hydroxy-2'-deoxyguanosine in the low zinc group. While evidence for DNA damage in the low zinc group was obtained, the activities of several antioxidant enzymes were similar between the low zinc and control groups. In summary, infants born to monkeys fed low zinc diets are characterized by evidence of DNA damage shortly after birth; this damage may be due to an increased rate of oxidative damage and/or a reduction in the rate of DNA repair.

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ABSTRACT. To investigate the effects of marginal zinc deficiency on early development, rhesus monkeys were fed a diet marginally deficient in zinc (M, 4 pglg) throughout pregnancy and during the first month of lactation. Despite the low concentration of zinc in the diet, M dams did not develop overt signs of zinc deficiency. However, compared to control dams fed diets adequate in zinc (C; 100 pg Zn/ g), M dams showed a low response to the mitogens concanavalin A and phytohemagglutinin. Pregnancy outcome was similar in the two groups and all of the neonates were judged to be healthy at delivery. From birth until d 30 of age, the infants were closely monitored for signs of zinc deficiency, and at d 30, they were killed and tissues were removed and analyzed for a number of parameters reported to be affected by zinc status. At birth, M infants had low plasma zinc concentrations compared to controls; however, this difference was not observed at d 30. D 30 M infants showed a normal response to the mitogens concanavalin A and phytohemagglutinin, but showed a low response to pokeweed mitogen. Tissue (liver, brain, spleen, kidney, and heart) trace element concentrations were similar in the two groups of infants, as were liver metallothionein concentrations and @Zn uptakelretention by isolated hepatocytes. Infant wt gain was inversely correlated with plasma zinc, liver zinc, and liver metallothionein concentrations in both the M and C groups. These results demonstrate that feeding a diet containing 4 fig zinclg to rhesus monkeys during pregnancy and lactation does not result in marked signs of zinc deficiency, although subtle signs occur in both the mother and infant. The data also support the concept that infant growth is associated with a depletion of tissue zinc stores. (Pediatr Res 26:470-477, 1989)

To determine if prenatal zinc deficiency has a persistent effect on metallothionein (MT) regulation, Swiss-Webster mice were mated and fed a diet containing either control (100 pg Zn/g) or low levels of zinc ( 5 pg Zn/g) from Day 7 of gestation to parturition. After birth all mice were given the control diet. Liver zinc and MT levels were 50% lower in newborn pups from dams fed the low zinc diets than in control pups. In control pups, liver zinc and MT concentrations were relatively stable during the first week of postnatal life. In contrast, in pups prenatally deprived of zinc, liver levels of zinc and MT increased such that by Day 3 of postnatal life, the levels were not significantly different from controls. At Day 56, serum IgM concentrations were significantly lower in the low zinc offspring. Liver zinc concentrations in the two groups of mice were similar at Day 70 postnatal, and in both groups liver MT levels were below detection limits. However, when Day 70 mice were given zinc injections to stimulate MT synthesis, the prenatally zinc deprived offspring showed markedly higher liver MT levels than did control mice given similar injections, despite similar liver zinc concentrations in the two groups. These results show that prenatal zinc deficiency has pronounced effects on postnatal MT metabolism which can persist into adulthood. o