[Free radicals and cytotoxicity of ethanol over human leucocytes in peripheral blood]

The ingestion of alcohol produces oxydative stress generating free radicals of oxygen and ethanol. These free radicals have a molecular reactive ability and, therefore, they play an important role in the production of the injury which appears in the liver and in other organs and tissues. We have done an "in vitro" study where we analyse the oxydative status at rest and the respiratory explosion produced by ethanol at final concentrations of 50 and 25 mM and by the phagocytosis of a previously opsonized concentrate of bacteria (E.coli) in human leucocytes taken from peripheral blood of six healthy persons.

We have used 1.2.3. dihydrorhodamine (non-fluorescent) as the oxydative marker because it is transformed in rhodamine (fluorescent), which is quantitatively studied by Flow Cytometry.

The peak of oxydative stress is reached with the bacteria in the phagocytes (monocytes 50% and granulocytes 90%) and it has a significant difference with the control group. By adding ethanol at 50 mM we have seen an statistic significant difference in oxydative stress in the cells of all three types (lymphocytes 9.19%, monocytes 32% and granulocytes 36%). With a concentration of 25 mM of ethanol the oxydative stress is increased but without a significant difference (lymphocytes 2.39%, monocytes 9.22% and granulocytes 4.46%). We have also seen toxic cellular effect which reaches the 40.75% of cells with ethanol at 50 mM, the 10.7% with ethanol at 25 mM and the 5.65% with bacteria.

The oxydative stress caused by the production of oxygen and ethanol free radicals in the leucocytes, and the proved cytotoxic effect of ethanol may play an important role over the qualitative and the quantitative leucocyte disorder on different organs and tissues of the alcoholic patient.