Influence of Marginal Maternal Zinc Deficiency on Pregnancy Outcome and Infant Zinc Status in Rhesus Monkeys

Abstract

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)

Adverse effects of parental zinc deficiency on metal homeostasis and embryonic development in a zebrafish model

“…Our results show that parental zinc deficiency causes their progeny to be compromised in zinc status and have alternations in expression of MTF-1 and specific zinc transporters. This is consistent with results in other model organisms where maternal zinc deficiency was associated with lower amounts of zinc in their offspring’s liver or plasma [57, 62, 63]. Also, given MTF-1’s important role in regulating metallothioneins and metal homeostasis in relationship to heavy metal exposure, it is possible that zinc deficiency, either in the parent or the embryo, may cause embryos to be more sensitive to toxic metals.…”

Aspects of neonatal metabolism of trace metals

“…In rats, deprivation of zinc during pregnancy reduces their pups' hepatic zincmetallothionein content and degradation of these complexes is accelerated (40). Similar phenomena have been noted in the rhesus monkey neonate (41).…”

Nutritionally Mediated Programming of the Developing Immune System

“…These findings may reflect glucocorticoid-mediated changes in the number or function of lymphocyte precursors (151)(152)(153)(154). Altered lymphocyte counts or function have also been reported in the animal literature regarding in utero exposure to nutrient deficiencies (337)(338)(339). One recent study indicated that fetal exposure to vitamin A deficiency can affect early progenitors, resulting in smaller B1a and B1b lymphocyte populations (212).…”