Cytogenetic effects of acetaldehyde in lymphocytes of Germans and Japanese: SCE, clastogenic activity, and cell cycle delay.

Acetaldehyde, the first metabolite of ethanol oxidation, caused a dose-dependent linear increase in the induction of sister chromatid exchanges in lymphocytes from both Germans and Japanese. Japanese, possessing only aldehyde dehydrogenase II isozyme (ALDH I deficient phenotype) and showing adverse effects after alcohol ingestion, did not differ in SCE rates from Germans and Japanese possessing isozymes I and II. At acetaldehyde concentrations above 360 microM, a significant chromosome breaking effect and a definite delay in cell cycle events, as evaluated by the BdUrd labeling technique, was registered in all individuals. Pyridoxal 5'-phosphate showed no protective effect against acetaldehyde-induced SCE formation in our system. A 24-h extension of the normal culture period revealed significantly higher rates of SCE at acetaldehyde doses above 360 microM.