Maternal Zn Research Articles

Breeding-Hen and Progeny Performance When Hens Are Fed Excessive Dietary Zinc

Short-term (12 wk) and long-term (44 wk) studies were conducted to observe the effects of excessive Zn supplementation on the performance of breeding hens and their progeny. Zinc sulfate was added to a corn-soybean meal diet containing 28 mg of Zn/kg in order to provide Zn supplementation at 0, 20, 200, and 2,000 mg/kg. Each dietary treatment was fed to two groups of 20, Single Comb White Leghorn hens and one New Hampshire rooster. The hens were 56-wk old at the start of the short-term study and 24-wk old when the long-term study began. Determinations were made for: fertility, hatchability, progeny growth to 3 wk of age, Zn-related feather-fraying among the progeny as well as Zn, Cu, and Fe in the liver, pancreas, and right tibiotarsus. The Zn treatments had no effect on hen performance or on reproductive performance. Even though Zn was considerably elevated and Cu was reduced in the eggs collected from hens fed the highest level of Zn, chick performance and the tissue content of Zn, Cu, and Fe were not influenced by the maternal Zn nutritional status.

Influence of maternal dietary Zn intake on expression of diabetes-induced teratogenicity in rats.

Diabetic rat pregnancies are characterized by altered maternal and fetal Zn metabolism and a higher frequency of fetal malformations. In this study, the effect of varying maternal dietary Zn on pregnancy and fetal outcome and on maternal and fetal trace element status were investigated. Starting on day 0 of gestation, streptozocin-induced diabetic and nondiabetic control rats were fed a low-Zn diet (4.5 micrograms/g diet), an adequate-Zn diet (24.5 micrograms/g diet), or a high-Zn diet (500 micrograms/g diet) throughout gestation. Fetuses were taken by cesarean section on gestation day 20. Fetuses from diabetic dams were smaller, weighed less, and had less calcified skeletons and more malformations than fetuses from control dams. In the controls, maternal dietary Zn had a minor effect on fetal malformation frequency. In contrast, in the diabetic animals, the low-Zn diet had a strong teratogenic effect. In diabetic dams, the adequate- and high-Zn diets improved fetal length and weight more than it did in fetuses from nondiabetic dams. However, supplemental dietary Zn during diabetic pregnancy did not further improve malformation frequencies. Liver and kidney Zn, Cu, and metallothionein concentrations were higher in diabetic dams than in control dams. In contrast, liver Zn, Cu, and metallothionein concentrations in fetuses of diabetic dams were lower than in fetuses from control dams, regardless of maternal dietary Zn intake. These results show that diabetes during pregnancy can amplify the teratogenic effects of a mild maternal Zn deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of maternal mineral deficiency on the hepatic metallothionein and zinc in newborn rats.

The effects of maternal Zn, Cu, or Fe deficiencies during late gestation on hepatic levels of metals and metallothionein (MT) and the binding of Zn and Cu to protein fractions were investigated in newborn rats. Timed pregnant rats were fed one of the following diets: Zn deficient (Zn-D), Cu-D, Fe-D, or control from day 12 of gestation until birth. The specific nutritional deficiency status of the dams was confirmed by low plasma levels of the deficient metal. Livers from pups were analyzed for MT, metal content, and metal-protein binding. Maternal Zn-D resulted in a greater than 50% reduction of hepatic MT levels in pups, whereas Cu-D and Fe-D had no significant effects. Pups in each deficient group showed a significant decrease in the hepatic levels of the respective metals. Fractionation of hepatic cytosols from the pups by Sephadex G-75 gel filtration showed that in both Fe-D and Cu-D pups the respective metals were depleted from the high molecular weight protein fraction, whereas in Zn-D pups the Zn was depleted mainly from the MT fraction (Ve/V0 approximately 2). Incorporation of [35S] cysteine into MT fractions was significantly lower in Zn-D pups as compared with control pups. These results indicate that there is a specific effect of the maternal Zn-D on the hepatic storage of Zn as MT in newborn rats.

Zinc deficiency in pregnant Long-Evans hooded rats: teratogenicity and tissue trace elements.

The Long-Evans hooded rat is widely used in experimental teratology. This study determines the teratogenicity of maternal Zn deficiency in the Long-Evans hooded rat, and examines the effects of Zn deficiency on Zn, Fe, and Cu concentrations in maternal and fetal tissues. Dams were fed an egg white-based diet containing 100 micrograms/g Zn for 1 week prior to mating. At mating rats were fed diets with 0.5, 4.5, 9.0, or 100 micrograms/g Zn ad lib, or 100 micrograms/g Zn pair-fed to 0.5 micrograms/g Zn dams. Laparotomies were performed on day 21 of gestation. Live fetuses and resorptions were counted. Fetuses were weighed and examined for external malformations. Some fetuses were used for Zn, Fe, and Cu determinations, others for internal or skeletal examination. Zn, Fe, and Cu levels were determined in maternal liver, kidney, and plasma. The 0.5 micrograms/g Zn dams lost weight during pregnancy; 27% of implantation sites were resorbed, 91.7% of live fetuses were malformed, and fetal weight was low. There were no malformed fetuses in the 4.5 micrograms/g Zn or 9.0 micrograms/g Zn groups; litter weights were low in the 4.5 micrograms/g Zn group. Tissue Zn was correlated with dietary Zn. Increased Fe concentration occurred in all maternal and fetal tissues in the 0.5 micrograms/g Zn group. The teratogenicity of Zn deficiency in the Long-Evans rat appears similar to that previously reported in the Sprague-Dawley strain.

TOENAIL ZINC (Zn) IN MOTHERS OF PROGENY WITH NEURAL TUBE DEFECTS (NTDS)

Diet-induced Zn deficiency in pregnant rats is known to cause cong. malfs. in 90-100% of their progeny, some 3% having spina bifida(SB).Mothers of children with SB have been reported to have high concentrations of hair Zn. Recent UK claims suggest vitamin A/folic acid periconceptional supplementation dramatically reduces the rate of recurrence of NTDs in women at risk.Because animal data have established a consistent relation between low plasma vitamin A and Zn deficiency, we studied the Zn status of women with a NTD fetus.Toenail clippings obtained mostly between 18-24 wks gestation provides a valuable retrospective assessment of maternal Zn status in the months prior to & around the periconceptional period.Zn analyses of toenails were performed by neutron activation analysis on 35 patients.21 controls (7 matched normal pregnancies, 14 normal females & males) had a normal range for Zn of 79.6-125 ppm.10 mothers with NTD fetuses, 2 with omphalocele, & 2 with with exogenous Zn intake were analyzed. High Zn values were found in 2 with SB fetuses (181;144), 1 with anencephaly (Anen.)(213), & 2 with Zn intake (208.4;290.8).Lowest value of all 35 was 1 with anen.(62.3).2 with SB+other malfs., 2 with Anen, 1 with lone SB all had normal Zn.In Zn deficiency both decreased and paradoxical increased Zn values have been found in hair.The consonance of our findings of high (3) or low(1) toenail Zn values among 10 mothers with NTD fetuses, suggests an abnormality in Zn metabolism in some women who bear children with NTDs.

Zinc nutritional status during pregnancy: a longitudinal study

Dietary zinc (Zn) intake and selected biochemical indices of Zn status were studied longitudinally at monthly intervals in 46 pregnant middle-income women, 10 of whom received a daily supplement of 15 mg Zn. Mean dietary Zn intake for the nonsupplemented subjects (group A) was 11.3 ± 4.1 mg/day (56% of the Recommended Dietary Allowances), and for the Zn-supplemented subjects (group B) was 21.7 mg/day (109% of the Recommended Dietary Allowance), including an average intake of 11.1 mg/day as supplemental Zn. The mean plasma Zn concentration of group A at 2 months gestation, 71.4 ± 9.8 μg/dl, was 17% lower than that of nonpregnant control women, and continued to decline significantly (p < 0.01) between 2 and 10 months gestation. Plasma Zn of group B did not differ significantly from group A at any stage of gestation. Mean serum alkaline phosphatase activity of group B was higher than that of group A at 7 of 8 months studied (p < 0.05). The level of prenatal iron supplementation in group A was negatively correlated with alkaline phosphatase activity and plasma Zn in the 2nd and 3rd trimesters, respectively. It is concluded that an early and progressive decline in plasma Zn which is not influenced by Zn intake occurs during gestation. Tentative standards for lower limits of normal at monthly intervals have been suggested. The higher alkaline phosphatase activity of group B compared with group A suggested that the dietary Zn intake of the latter was suboptimal. Prenatal supplemental iron may adversely affect maternal Zn status.