The protective effect of vitamin E against prenatal and early postnatal ethanol treatment-induced heart abnormality in rats: a 3-month follow-up study.

Abstract

Ethanol consumption during pregnancy is associated with fetal heart malformation. However, the underlying mechanism of prenatal ethanol exposure causing heart malfunction is not well known. The current study examined the effect of prenatal and early postnatal ethanol consumption on heart abnormality resulting from oxidative and inflammatory stress. It was also intended to find out whether vitamin E inhibits the abnormality induced by ethanol in rats' heart tissue. Pregnant Wistar rats received ethanol with/without vitamin E from the seventh day of gestation (GD7) throughout lactation. The proliferation in heart muscle cells and coronary smooth muscle cells, protein carbonyl, IL-6, TNF-α, homocysteine levels, also lipid profile in heart and plasma of male pups were measured at the end of lactation (PN 21) and 90 days after birth (PN 90). The results indicated proliferation of heart muscle and coronary smooth muscle cells along with heart structural alteration, protein oxidation, lipid peroxidation, inflammatory reaction, and hyperhomocysteinemia in offspring after 21 and 90 days of birth compared with the controls. Vitamin E treatment significantly decreased cell proliferation and heart structural alteration, compared with the group treated by ethanol alone. Furthermore, it reduced the elevation of protein carbonyl, lipid peroxidation, and increased inflammatory proteins to levels as those of the controls. These findings strongly support the idea that ethanol intake by dams during pregnancy and early postnatal days induces heart abnormality mediated by oxidative stress and inflammatory reactions, and that these effects can be alleviated by using vitamin E as an antioxidant and anti-inflammatory molecule.