Molecular Basis for Abnormal Parturition in Zinc Deficiency in Rats

Abstract

Apgar (1968a) was the first to recognize that female rats fed a diet containing 1 μg Zn/g diet throughout gestation experienced difficult and prolonged labor accompanied by excessive bleeding. Placentae were left unconsumed and neonates were abandoned rather than cleaned and nursed. Further studies by Apgar (1968b, 1970, 1972, 1973, 1975, 1976, 1977a,b) showed that such effects were relatively specific for zinc since they did not appear in restricted-fed rats or in rats fed diets low in protein, thiamine, copper or manganese. Moreover, they observed that the typical syndrome still developed when the low-zinc diet was begun as late as day 18 of gestation and could be prevented by zinc repletion instituted on day 19 in rats offered the low-zinc diet from mating. O’Dell et al., (1977) reported that zinc-deficient dams also exhibited a significant decrease in body temperature (38.3° vs 36.9° C), hypotension (115 vs 90 mm Hg) and delayed, as well as prolonged, parturition. Others have reported toxic effects during late pregnancy in rats fed diets containing a high content of phytate, a substance well known to bind zinc and make it unavailable for absorption (Eklund, 1973; McLaughlan et al., 1975; Anderson et al., 1976). During the course of studies in our laboratory in 1977 on the effect of nutrition on lens development, we employed a mineral mix that contained only 3–5 μg Zn/g diet, an amount that we expected to be sufficient. Upon observing the syndrome described above, we became aware of this unique effect of zinc and decided to attempt to determine its molecular basis.