The effects of alcohol on bone marrow are not well understood. We measured the influence of ethanol and its metabolite, acetaldehyde, on the in vitro proliferation of hematopoietic progenitor cells from mice and human beings. Colony formation by both early and late erythroid progenitor cells was suppressed by concentrations of ethanol (0.05 to 0.2 per cent) that are easily achieved in vivo. The corresponding suppressing concentration of acetaldehyde was 0.001 per cent. In contrast, suppression of granulocyte/macrophage progenitor cells required 3.0 per cent ethanol or 0.03 per cent acetaldehyde. Spleen colony formation by pluripotent stem cells was resistant to concentrations of ethanol and acetaldehyde that suppressed in vitro colony formation of committed myeloid and erythroid progenitor cells by 50 per cent. The suppression of both myeloid and erythroid colony formation was partially reversed by supplementing the cultures with folinic acid or pyridoxine. These data provide an explanation for the preferential suppression of erythropoiesis observed clinically in ethanol abuse. They also suggest that acetaldehyde has a role in ethanol-mediated bone-marrow suppression. (N Engl J Med. 1982; 307:845–9.) ALTHOUGH ethanol is widely used for its mood-altering effect, it is a toxic substance that directly or indirectly causes impairment of cellular function in every organ of the body. Within the bone marrow, no cell line is impervious to the influence of the drug. Acutely, ethanol ingestion produces vacuoles in erythroid and myeloid progenitor cells1 and causes thrombocytopenia.2 By substituting for nutritious calories and impairing folate metabolism,3,4 chronic ethanol ingestion leads to megaloblastic hematopoiesis. In addition, ethanol interferes with iron utilization by red cells,4 resulting in hyperferremia and excess erythrocyte mitochondrial iron accumulation.5 The latter abnormality may be potentiated by.
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