[The action of oxidative stress induced by ethanol on the central nervous system (CNS)]. / Wplyw stresu oksydacyjnego indukowanego etanolem na osrodkowy uklad nerwowy (OUN).

The brain is an organ which metabolically consumes about 20% of the total oxygen received by the organism. This causes the generation of free radicals, especially in the presence of some xenobiotics, such as ethanol. In order to prevent free radical-induced cellular damage, the organism developed a defense mechanism, the antioxidative system. The content of both exogenous and endogenous antioxidants in the central nervous system (CNS) is very small in comparison with that of other tissues, which in relation to the high level of polyunsaturated fatty acids (PUFAs) makes the CNS exceptionally susceptible to free-radical damage. The antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GSSG-R) are present in the CNS i.e. in the cortex, cerebellum, hypothalamus, striatum, and spinal cord, where they are responsible for the brain's basic functions, both physical and cognitive. Moreover, the highest activity of these enzymes is observed in neurons and/or glial cells. The activity of antioxidant enzymes is significantly changed in the CNS of animals chronically intoxicated with ethanol. The decrease in these activity may indicate at oxidative modification of the enzymatic proteins caused by free radicals which are generated during ethanol and acetaldehyde metabolism. It may also be caused by the decrease in the synthesis rate of these enzymes. However, the increase in the activity of antioxidant enzymes may often be explained as an adaptive reaction to an excess production of free radicals. The catalase is an exception in this respect because the decrease in its activity is related to the enhancement of protein synthesis. Ethanol intoxication also caused a decrease in GSH concentration, especially in the cerebellum, striatum, and cortex. This may be explained by the increase in the concentration of acetaldehyde, which is removed from cells with the use of this antioxidant. The antioxidative abilities of the CNS also depend on exogenous antioxidants which are provided to the organism during food intake. The most important exogenous antioxidant in the CNS is vitamin E. The content of vitamin E as well as that of vitamin C in the CNS is decreased, whereas the content of vitamin A is increased after ethanol administration. The high vitamin A level may cause damage of the central nervous system, especially in young rats exposed to ethanol in the prenatal period.

Green tea supplementation in rats of different ages mitigates ethanol-induced changes in brain antioxidant abilities.

Oxidative stress induced by chronic ethanol consumption, particularly in aging subjects, has been implicated in the pathophysiology of many neurodegenerative diseases. Antioxidants with polyphenol structures, such as those contained in green tea, given alone for 5 weeks in liquid Lieber de Carli diet followed by administration with ethanol for 4 weeks with ethanol have been investigated as potential therapeutic antioxidant agents in the brain in rats of three ages (2, 12, and 24 months). Ethanol consumption caused age-dependent decreases in brain superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities. In addition, ethanol consumption caused age-dependent decreases in the levels of GSH, selenium, vitamins, E, A and C, and beta-carotene and increases in the levels of oxidized glutathione (GSSG). Changes in the brain's antioxidative ability were accompanied by enhanced oxidative modification of lipids (increases in lipid hydroperoxides, malondialdehyde, and 4-hydroxynonenal levels) and proteins (increases in carbonyl groups and bistyrosine). Reduced risk of oxidative stress and protection of the central nervous system, particularly in young and adult rats, after green tea supplementation were observed. Green tea partially prevented changes in antioxidant enzymatic as well as nonenzymatic parameters induced by ethanol and enhanced by aging. Administration of green tea significantly protects lipids and proteins against oxidative modifications in the brain tissue of young and adult rats. The beneficial effect of green tea can result from the inhibition of free radical chain reactions generated during ethanol-induced oxidative stress and/or from green tea-induced increases in antioxidative abilities made possible by increases in the activity/concentration of endogenous antioxidants.