The research was performed in vitro on human blood erythrocytes isolated from blood taken on EDTA (SOD) or heparine (GPx). The SOD activity was measured with Ransod test (Randox), GPx with Ransel (Randox). The concentration of ethanol was 0,4-2,4mg/ml; 17-β-Estradiol 0,75nM, 1,5,10μM. The results were evaluated with statistical analysis (program Statistica 8.0)with Anova or T-Student's test.

    It was observed, that ethanol in conc. 0,5 and 2,0mg/ml significantly (p<0,05) increased the activity of SOD and GPx in the comparison to the control. The effect of ethanol acute intoxication is quite different then one observed in long-lasting exposure, specially the addiction (decrease). 17-β-Estradiol in physiological level (0,75nM) didn't influence on SOD activity, but in higher conc. (1,0 and 5,0μM) significantly (p<0,001) decreased enzyme activity. Similarly estradiol in every examined concentration decreased the GPx activity in erythrocytes. The joint effect didn't show the interaction. The action of estradiol with every concentration of ethanol was comparable with the control. Because ethanol itself increased the enzymes activity, the inhibiting effect of estradiol on oxidative stress caused by ethanol is noted. It is known that oxidative stress stimulate the activity of natural defence system SOD and GPx. The lack of stimulation could be the result of oxidtaive stress inhibition, however the direct effect of xenobiotics on enzyme can't be excluded.

    In summary it seems that estradiol partly reduces oxidative stress caused by ethanol in the influence on natural enzymatic barrier activity.

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