Ethanol-mediated fetal dysmorphology and its relationship to the ontogeny of maternal liver metallothionein.

Background: Fetal zinc (Zn) deficiency arising from ethanol-induction of the Zn-binding protein metallothionein (MT) in the mother's liver has been proposed as a mechanism of teratogenicity. Here, we determine the ontogeny of MT and Zn homeostasis in rats and mice and then examine the effect of acute ethanol exposure in early embryonic development on this relationship. The protective effect of Zn against ethanol-mediated fetal dysmorphology is also examined.

Dietary zinc supplementation throughout pregnancy protects against fetal dysmorphology and improves postnatal survival after prenatal ethanol exposure in mice.

Background: We have previously demonstrated that ethanol teratogenicity is associated with metallothionein-induced fetal zinc (Zn) deficiency, and that maternal subcutaneous Zn treatment given with ethanol in early pregnancy prevents fetal abnormalities and spatial memory impairments in mice. Here we investigated whether dietary Zn supplementation throughout pregnancy can also prevent ethanol-related dysmorphology.

Methods: Pregnant mice were injected with saline or 25% ethanol (0.

Maternal dietary zinc supplementation prevents aberrant behaviour in an object recognition task in mice offspring exposed to LPS in early pregnancy.

Maternal infection during pregnancy is associated with an increased risk of neurodevelopmental damage. While the mechanism is unclear accumulating evidence suggests that the maternal inflammatory response may be responsible. Metallothionein (MT) is a zinc (Zn)-binding protein that when induced in the mother's liver during the acute phase response has been found to cause a fetal Zn deficiency.

Dietary zinc supplementation during pregnancy prevents spatial and object recognition memory impairments caused by early prenatal ethanol exposure.

Alcohol-induced zinc (Zn) deficiency is one of the mechanisms proposed as a cause of ethanol teratogenicity. Subcutaneous Zn treatment with ethanol in early pregnancy has been shown to prevent birth abnormalities and memory impairments in mice. This study examined whether dietary Zn supplementation throughout pregnancy can prevent cognitive impairments caused by early ethanol exposure.

Prenatal zinc treatment at the time of acute ethanol exposure limits spatial memory impairments in mouse offspring.

Zinc (Zn) treatment given together with acute ethanol in early pregnancy has previously been demonstrated to protect against physical birth abnormalities in mice. The current study examined whether this Zn treatment (s.c.