Effects of ethanol, nicotine and caffeine gestational exposure of female rats on lung and brain tissues in fetuses: morphological and biological study

Aim: The purpose of this study was to evaluate the implications of toxic exposure on pregnancy, by exploring the oxidant-antioxidant balance and the histopathological (HP) changes of fetal organs. Materials and Methods: Our study was performed on fetuses of gestating rats exposed to ethanol, nicotine and caffeine. HP tissue analysis of fetuses' brain and lung samples were performed. Brain and lung homogenates were quantitatively analyzed to determine the oxidant-antioxidant balance [malondialdehyde (MDA), protein carbonylation (PC), glutathione (GSH) and thiol groups (-SH)]. Results: An increase in cerebral pro-oxidant capacity was observed for alcohol exposure groups through increased MDA levels (p<0.001), as compared to controls. An increase in pulmonary and cerebral pro-oxidant capacity was observed for nicotine and caffeine study groups, through increased PC levels (p<0.001). Lower GSH levels indicate a decrease in brain antioxidant defenses in alcohol, nicotine and caffeine groups. Alcohol and nicotine exposure in pregestational and gestational periods caused neuronal hypoplasia in hippocampus and brainstem congestion. Caffeine registered negligible differences as compared to controls. Conclusions: In our experimental model for gestational exposure to chemical agents, alcohol was the strongest teratogenic agent in rat brain samples. No significant changes were observed in lung samples. Results indicate an increase in oxidative stress as a result of alcohol and nicotine consumption during gestation in rats.