Cellular necrosis in zinc‐deficient rat embryos

Abstract

Abnormal cellular necrosis was studied in 9.5-11.5-day embryos obtained from zinc-deficient rats. At periods of low maternal zinc status induced by a high intake of a zinc-deficient diet, cell death was observed in those regions of the embryo that were most sensitive to teratogenic insult at that time. As the maternal serum zinc level increased during the fasting phase of the feeding cycle, the degree of necrosis decreased, leaving the tissue histologically more normal even though the embryos were grossly malformed. The mitotic index of cells in the neural epithelium and limb buds of zinc-deficient, non-necrotic embryos was found to be elevated, but there was no evidence of blockage at any particular stage of mitosis. It can be hypothesised that during the early stages of organogenesis, periods of low maternal zinc status initiate unscheduled cell death by some as yet undefined mechanism that in turn, gives rise to the morphological anomalies observed later.

Prenatal Zinc Deficiency: Influence on Heart Morphology and Distribution of Key Heart Proteins in a Rat Model

“…As congenital heart defects, the most common type of structural birth defects [66,67], are known to result from genetic and environmental insults interactions, these data are relevant, as they suggest that maternal Zn status can be a modulating factor in determining an unfavorable outcome when a genetic susceptibility is already present. Similar to those previously reported by our group and others [5,9,68], the teratogenic outcomes that we observed in fetuses from dams fed the ZnD diet involved heart structures and vascular segments, where normal development depends on the proper infiltration and differentiation of cardiac NCC, and included, but were not limited to, other tissues populated by NCC such as the face (lip, palate, and eyes) and the thymus. As Zn depletion can lead to caspase 3 activation and increased cell death [14,17,69], we investigated the idea that developmental Zn deficiency has reduced the population of NCC targeting to the heart.…”

Pathogenesis of bromodeoxyuridine‐induced cleft palate in hamster

“…A transient appearance of lysosomes in a variety of embryonic tissues following exposure to numerous chemicals has also been observed in various teratological studies (Jurand, 1966;Schweichel and Merker, 1973;Morriss, 1973;Merker et al, 1975;Theodosis and Fraser, 1978;Langman and Cardell, 1978;Peters et al, 1979;DeSesso, 1981;Kuchta, 1982;Manson et al, 1982;Rooze, 1982;Record et al, 1985;Sulik et al, 1988). It was assumed that the appearance of lysosomes was an expression of cell death.…”

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

“…In the mother, the periods of a high intake of the zinc-deficient diet are associated with low maternal plasma zinc concentrations that can adversely affect the embryo. Embryos taken during gestation at a high point of maternal food intake (e.g., relatively low plasma zinc) have been reported to exhibit increased cell death characteristic of apoptosis (Record et al, 1985;Rogers et al, 1995). During periods of low food intake, e.g., semi-fasting state, the catabolism of maternal tissues results in mobilization of zinc such that plasma zinc rises (though concentrations are typically still at values that are lower than those of zinc adequate controls) (Masters et al, 1983;Record et al, 1986).…”