Expression of the mouse metallothionein-I and -II genes provides a reproductive advantage during maternal dietary zinc deficiency

被引:55
作者
Andrews, GK [1 ]
Geiser, J [1 ]
机构
[1] Univ Kansas, Med Ctr, Dept Biochem & Mol Biol, Kansas City, KS 66160 USA
关键词
knockout; mice; metallothionein; pregnancy; zinc deficiency;
D O I
10.1093/jn/129.9.1643
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
The function of metallothionein in zinc homeostasis was examined by using mice homozygous for knockout (KO) of the metallothionein-I or -II (MT-I and MT-II) genes. Pregnant MT-I/II KO mice or control mice were fed a zinc-deficient (1 mu g/g or 5 mu g/g) diet or a zinc-adequate (50 mu g/g) diet during specific periods of pregnancy, and the effects on morphogenesis of the embryos were determined at day 14 of pregnancy (day 1 = vaginal plug). In the homozygous MT-I/II KO, as well as in the nontransgenic control mice, severe dietary zinc deficiency (1 mu g/g) beginning on day 1 of pregnancy was embryotoxic acid teratogenic, and the majority of the embryos in both strains were dead by mid-gestation. However, 53% of the surviving embryos in the MT-I/II KO mice were morphologically abnormal compared to only 32% of the embryos in the control mice. In subsequent experiments, moderate dietary zinc deficiency (5 mu g/g beginning on day 1 of pregnancy or 1 mu g/g dietary zinc beginning on day 8 of pregnancy) exerted teratogenic, but not embryotoxic effects. Embryos in the MT-I/II KO mice were 260 to 290% as likely to develop abnormally than were embryos in the control mice fed these same diets. These results demonstrate that the expression of the MT-I and -II genes in pregnant females improves reproductive success during maternal dietary zinc deficiency.
引用
收藏
页码:1643 / 1648
页数:6
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