Ethanol exposure in prenatal and early postnatal induced cardiacinjury in rats: involvement of oxidative stress, Hsp70, ERK 1/2, JNK,and apoptosis in a 3-month follow-up study

Alcohol exposure during pregnancy induces a wide range of structural and functional abnormalities in the fetal heart. However,the underlying mechanism of this phenomenon is not well known. This study was undertaken to elucidate probable mechanismsof myocardial damage induced by prenatal and early postnatal ethanol treatment. Pregnant Wistar rats received ethanol 4.5 g/kgBWonce per day from the seventh day of gestation (GD7) throughout lactation. The oxidative stress injury of the myocardium inpups was evaluated by measuring levels of oxidative stress biomarkers. Histopathological examinations and Western blot wereperformed to evaluate histological features, apoptosis, and molecular alterations in the myocardial tissue of male pups on thepostnatal day 21 (PN-21) and postnatal day 90 (PN-90). The results showed that maternal ethanol consumption caused oxidativestress (impaired total antioxidant capacity and malondialdehyde), histological changes, and apoptosis of the myocardium in thepups on PN-21 and PN-90. At the molecular levels, Western blot analysis revealed that ethanol modulated the protein expressionof p-ERK1/2, p-JNK, and Hsp70 in the myocardial tissue of the pups after 21 and 90 days of birth compared with the controls.These findings revealed that maternal ethanol intake induced cardiac toxicity in part, mediated by oxidative stress and apoptosisin the pups. A further mechanism study revealed that ethanol enhanced ERK1/2 and JNK phosphorylation and Hsp70 proteinexpression.