# ZINC DEPRIVATION AND TERATOGENESIS

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA AT DAVIS · 1994 · $328,442

## Abstract

Suboptimal dietary zinc deficiency is a potential etiological risk factor
for pregnancy complications and neonatal development.  Our laboratory has
focused on the role of dietary zinc deficiency in pregnant rhesus monkeys
to understand the mechanisms that lead to a "nutritionally-at-risk"
pregnancy.  Our data indicate that the effects of zinc deprivation are most
marked during periods of growth and development.  During the next five
years we will continue our use of the rhesus monkey to define mechanisms
that predispose to a "nutritionally-at-risk" pregnancy.  In particular, we
will study the role of moderate zinc deprivation in adolescent rhesus
monkeys.  Adolescent rhesus monkeys are amongst the best models for human
adolescence.  We will investigate the effects of dietary zinc deficiency by
focusing on the extent to which zinc deficiency influences growth and
sexual maturation via effects on growth factors and other hormones.  More
importantly, utilizing pregnant animals, both the mother and conceptus will
be studied to identify basic biochemical and cellular lesions associated
with zinc deficiency.  We postulate that the health of adolescent females
will be significantly disrupted by concurrent dietary zinc deficiency and
will involve defects in the release, distribution, binding, or/or tissue
response to growth factors.  We also postulate that concurrent
abnormalities will be seen in immunological and behavioral function.
Additionally, we believe that embryonic and fetal zinc deficiency can arise
as a consequence of acute phase reactions which disrupt maternal zinc
homeostasis.  We propose that acute phase reactions, such as that mediated
by administration of recombinant TNFalpha, will lead to the so-called
"maternal toxicity syndrome" and will include a sequestering of zinc in
maternal liver due to enhanced production of the acute phase protein
metallothionein coupled with an enhanced uptake of zinc into liver due to
an increase in plasma alpha2 macroglobulin.  The consequence of these
events will be reduced zinc transfer to the embryo/fetus.  The
abnormalities that occur are due to a number of factors including zinc
deficiency induced alterations in the rate and extent of cellular lipid,
nucleic acid and protein oxidation and altered methylation of DNA.  Support
for these hypotheses would have major health implications, both for zinc
supplementation during maternal toxicity/acute phase reactions as well as
for providing a unifying hypothesis for understanding the potential
interactions between multiple exogenous insults, zinc deficiency and
developmental abnormalities.

## Key facts

- **NIH application ID:** 2197084
- **Project number:** 5R01HD014388-14
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **SAM.gov UEI:** TX2DAGQPENZ5
- **Principal Investigator:** MERRILL E GERSHWIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1994
- **Award amount:** $328,442
- **Award type:** 5
- **Project period:** 1987-07-01 → 1995-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2197084

## Citation

> US National Institutes of Health, RePORTER application 2197084, ZINC DEPRIVATION AND TERATOGENESIS (5R01HD014388-14). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2197084. Licensed CC0.

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