Abstract
The effects of ethanol on the production of oxygen-derived free radicals by neutrophils are controversial. Osmolarity-mediated alteration of cell volume appears to be an important mechanism for regulating neutrophil activity. We investigated in neutrophils from healthy volunteers the effect of isotonic/hypertonic ethanol on both chemiluminescence amplified by a Cypridina luciferin analog in response to N-formyl-Met-Lue-Phe and cell volume measured with a Coulter counter. Both isotonic and hypertonic ethanol significantly decreased chemiluminescence in a dose-dependent manner. Isotonic ethanol produced a greater magnitude of inhibition than hypertonic ethanol (P < 0.01). Another permeable molecule, urea, and hypotonic solution had the same effects on chemiluminescence. Isotonic and hypertonic ethanol caused a prompt cell expansion and shrinking, respectively. On the other hand, isotonic sucrose, an impermeable molecule, was ineffective in both chemiluminescence and cell volume changes. These data suggest that isotonic ethanol inhibits the superoxide anion production by inducing cell expansion probably due to increased intracellular osmotic pressure caused by rapid ethanol permeation through the plasmalemma. This impaired neutrophil function may, in some part, contribute to the susceptibility to infection in alcoholics.
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