In utero exposure to tobacco and alcohol modifies neurobehavioral development in mice offspring: consideration a role of oxidative stress

Abstract

Objective: To determine whether in utero tobacco and alcohol exposure induces long-term neurobehavioral alterations and whether oxidative stress/damage is a possible causal factor. Methods: Gravid mice were subjected to tobacco smoking and alcohol consumption. Their offspring were subsequently evaluated in developmental and behavioral tests. Antioxidative enzymes and erythrocyte membrane fluidity of adult offspring were measured. Results: The intrauterine tobacco and alcohol exposure has resulted in significant reduced postnatal body and organ weights accompanied by reduced gestational body weight gain in their mothers. Such exposure also induced remarkable developmental delay in neonatal reflexes and notable behavioral deficit in adulthood, namely reduced motive coordination and locomotor activity as well as impaired learning and memory abilities. Furthermore, the formation of malondialdehyde (MDA) increased significantly whereas the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), catalase (Cat) and glutathione S-transferases (GST) decreased in the cerebral cortex and liver of prenatal intoxicated offspring. The embryonic intoxication also markedly reduced erythrocyte membrane fluidity in offspring. Conclusion: Our study shows the long-term neurotoxicity associated with prenatal tobacco and alcohol exposure, and suggests that the deleterious outcome may be in relation to increased free radicals formation and oxidative stress.