Alcoholism is known to accompany with hyperhomocysteinemia which can be a risk factor of cardiovascular and cognitive function impairment. Numerous metabolic and neurological effects of ethanol are associated with the influence of homocysteine on the NMDA receptors in neurons. Homocysteine is a toxic sulfur-containing amino acid which has been the subject of great interest in recent years. However, the acute effects of ethanol on the levels of sulfur-containing compounds including homocysteine has not been investigated yet.

We studied the influence of various doses of ethanol on the levels of cysteine, homocysteine, and reduced glutathione in both plasma and RBC of rats in short time after single intraperitoneal injection of ethanol.

Methods used: the compounds studied were determined by reversed-phase HPLC after pre-column derivatization with SBD-F and detection by fluorescence. Sulfur-containing compounds were reduced by TCEP from both plasma and haemolysed RBC, so total levels of the compounds were determined.

Results. We found no differences in the levels of cysteine and homocysteine with control group after all doses of ethanol used (1, 2,5, and 5 g/kg, 60 min) both in blood plasma and erythrocytes. However, acute ethanol intoxication with higher dose of ethanol (5 g/kg) led to an increase in the level of reduced glutathione in plasma but not in RBC compared to control and lower doses of ethanol.

We suppose that homocysteinemia occurring in chronic alcohol consumption in not direct metabolic consequence of ethanol intoxication but rather might be long-term shifts in the interrelationships in either expression or regulation of the methionine/homocysteine-metabolizing enzymes. We still have no satisfactory explanation for the very surprising finding of the significant increase in the plasma GSH level after administration of ethanol in very high dose which need further investigation.

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