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


CONCLUSIONS
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.
Department of Pharmacology, Medical College of Wuhan University, 430071, China.
Yan
Y
Li
Hui
H
Wang
D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development / Q000502:physiology; D001522:Behavior, Animal / Q000187:drug effects* / Q000502:physiology; D001724:Birth Weight / Q000187:drug effects; D002540:Cerebral Cortex / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000175:diagnosis; D005979:Glutathione Peroxidase / Q000737:chemistry / Q000378:metabolism; D008315:Malondialdehyde / Q000737:chemistry / Q000378:metabolism; D018811:Maternal Exposure / Q000009:adverse effects; D008431:Maternal-Fetal Exchange / Q000187:drug effects; D008560:Membrane Fluidity / Q000187:drug effects / Q000502:physiology; D051379:Mice; D009460:Neurologic Examination / Q000187:drug effects / Q000379:methods; D009929:Organ Size / Q000187:drug effects / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012907:Smoking / Q000009:adverse effects*; D015430:Weight Gain / Q000187:drug effects
D008315:Malondialdehyde; D005979:Glutathione Peroxidase