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Abstract
AimsThis study investigated the neurotoxic effects of prenatal alcohol and nicotine exposure in the cortex and hippocampus of rodents. Main methodsBehavioral alterations, electrophysiological changes, and biochemical markers associated with cholinergic neurotransmission, neural oxidative stress, mitochondrial function, and apoptosis were evaluated. Key findingsPrenatal alcohol exposure induced the generation of ROS, nitrite and lipid peroxide, decreased mitochondrial Complex-I and IV activities, increased Caspase-1 and 3 activities, had no effect on cholinergic neurotransmission, increased expression of PSD-95, decreased LTP and decreased performance on spatial memory tasks. However, nicotine exposure, in addition to alcohol exposure, was found to mitigate the negative effects of alcohol alone on ROS generation and spatial memory task performances. Furthermore, we also studied the role of ILK in prenatal alcohol and nicotine exposure. SignificancePrenatal Smoking and/or drinking is a major health concern around the world. Thus, our current study may lead to better insights into the molecular mechanisms of fetal alcohol and nicotine exposure on the developing offspring.
Highlights
A growing concern in developed countries is drinking during pregnancy
Alcohol and alcohol þ nicotine exposure increased the generation of reactive oxygen species (ROS) significantly in the cortex compared to the control (Figure 1a, p < 0.05)
With regard to the other antioxidant enzymes such as glutathione peroxidase, superoxide dismutase and catalase, prenatal exposure to alcohol and alcohol þ nicotine did not affect the glutathione peroxidase (Figure 1e), but there was a significant decrease in superoxide dismutase activity of both experimental groups compared to the control (Figure 1f)
Summary
A growing concern in developed countries is drinking during pregnancy. A large number of women (around 15%) have admitted to have consumed alcohol at some stage of their pregnancy. Alcohol is a serious teratogen that can cause problems associated with the CNS, such as hyperactivity, poor movement coordination and muscle control, lower than average IQ, and cognitive deficits [3] Some of these effects have been attributed to neuronal dysfunction in various regions of the brain of the offspring notably the hippocampus [4, 5], and children with FASD experience difficulty in spatial and memory tasks [6, 7]. Clinical and experimental trials have indicated a strong association between nicotine and alcohol use [13], pointing to their concurrent usage It appears that a significant population of women who consumes both these teratogens during pregnancy, yet a few clinical data exist on the cumulative effects of alcohol and nicotine on developing offspring [14]. We looked into some of these mechanisms in the present alcohol þ nicotine model
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