Abstract
Alcohol as a teratogen could induce foetal malfunction or foetal alcohol spectrum disorder by mechanisms involving the dehydrogenases, cytochrome P4502E1and catalase. These result in the concomitant reactive oxygen species (ROS) generation and the resultant ROS -related damage to the central nervous system of the developing foetus. Thus, alcohol-induced teratogenesis (and even other alcohol-induced adverse effects) were generally mediated via and/or characterized by oxidative stress, cell death, mitochondrial dysfunction, interference with the activity of growth factors and retinoic acid imbalance. In particular, ROS could overwhelm cellular activities by inactivating electron transport chain complex hence decreasing the production of mitochondrial energy and activating the apoptotic pathway. On the other hand, the use of N-Methyl-D-Aspartate receptors antagonists, antioxidants and neurotrophic factors seemingly attenuated alcohol-induced teratogenesis and other effects, hence served as its management strategies. L-Arginine, an amino acid that plays central role in the synthesis of nitric oxide improved foetal regulation of glucose release, transport and utilization which were fundamental to alcohol-induced damage. This suggested the possible ameliorative role of L-Arginine on alcohol-induced teratogenesis and other adverse effects of alcohol over use. Thus, the present review speculated that L-arginine could mitigate alcohol-induced teratogenesis and other adverse effects by enhancing the synthesis of the antioxidant molecule, nitric oxide, warranting detailed further studies. The outcome of such studies could help in managing and/or controlling alcohol-induced teratogenesis in women on alcohol prior to and/or during pregnancy as well as other adverse effects of alcohol in humans.
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