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Reversibility of Developmental Retardation following Murine Fetal Zinc Deprivation¹

Department of Internal Medicine, Section of Rheumatology/Clinical Immunology ^• Department of Nutrition, University of California, Davis, CA 95616

To investigate the effects and reversibility of moderate prenatal zinc deprivation, pregnant mice were fed, beginning on day 7 of gestation, a diet containing either 100 ppm (control) or 5 ppm zinc; pair-fed controls were also studied. Nutritional manipulation was limited to the prenatal period. Zinc-deprived dams had significantly smaller litters than did controls, and postnatal survival was markedly compromised. Progeny of zinc-deprived dams displayed significant growth retardation, as reflected by lower body weight and length than controls, whether ad libitum-fed or pair-fed. Growth of spleen and thymus was affected by zinc deprivation to a significantly greater extent than was growth of heart, kidney or brain. Cross-fostering of control pups to zinc-deprived dams resulted in delayed growth; however, retardation was not as great as that observed in deprived pups allowed to suckle their natural mothers. Cross-fostering of zinc-deprived pups to control dams improved growth of most organs, but did little to improve growth of spleen and, most notably, thymus. Zinc-deprived pups exhibited considerable "catch up" growth following neonatal zinc repletion, and by 6–8 weeks of age, no significant differences between control and deprived offspring were observed.

KEY WORDS: • zinc • fetal development • catch up growth • cross-fostering

¹ Supported in part by funds received from the Amociation for Children and Adults with Learning Disabilities and NIH grants CA-20616, CP-65845 and HD-01743.

² Recipient of a fellowship from the American Society for Clinical Nutrition.

³ Recipient of Research Career Development Award AI-00193.

Manuscript received 14 December 1981.

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