2018
Volume 18, Number 1, pp. 21–27
Alteration of rat redox status at low (hormetic) dose exposure to ethanol
T.V. Sanikidze, I.K. Svanidze, D.P. Museridze, L.G. Gegenava, N.N. Gvinadze and S.L. Kalmakhelidze
Department of Neurotoxicology, I. Beritashvili Centre of Experimental Biomedicine, Tbilisi, Georgia
During pregnancy the consumption of alcohol engenders foetal alcohol syndrome (FAS), manifested in numerous neurological diseases. Oxidative stress is a common mechanism of the harmful effects of alcohol intoxication. Consumption of low doses of ethanol is associated with positive events, and high doses with tissue damage. In this respect, ethanol can be considered as a classic example of hormesis, which is considered to be the basis for the mechanisms of adaptive reactions. The redox status of the offspring of rats was studied when the females consumed low (0.025 g/kg) and high (0.2 g/kg) doses of ethanol during pregnancy. Oxidative metabolism in the cortex of the offspring brain, liver and blood was investigated by electron paramagnetic resonance (EPR). For the detection of lipoperoxide (LOO·) and free nitric oxide (NO) radicals spin-traps were used. It was shown that the hormetic dose of ethanol did not change the intensity of oxidative metabolism in the offspring, but caused an ethanol dose-dependent activation of NO synthesis in the cerebral cortex. Prenatal intoxication (15% ethanol) of the offspring caused changes in oxidative metabolism in the cortex, characterized by mitochondrial electron transport chain disorders, and accumulation of lipid peroxides and NO.
Keywords: ethanol, free nitric oxide, hormesis, lipoperoxides, oxidative stress