Differential responses of human neural and hematopoietic stem cells to ethanol exposure.

The mechanisms underlying fetal developmental defects caused by maternal ethanol (EtOH) consumption remain unclear. The symptoms of fetal alcohol syndrome (FAS) include neurological and immunological dysfunctions that are linked to cell reduction in these systems. Neural (NSC) and hematopoietic stem cells (HSC) may be targets for the cytotoxic effects of EtOH. Furthermore, protein kinase C (PKC) signal transduction systems of these stem cells may be involved in EtOH-induced cell death. Purified CD34+ human fetal liver hematopoietic stem cells (HSC) and CD133+/nestin+ human neural stem cells (NSC) were exposed to 0.1-10 mM EtOH. A range of indices of cell damage indicated that these doses of EtOH were deleterious to NSC, but had no observable effects on HSC. Furthermore, the colony-forming ability of NSC was completely inhibited by 5 mM EtOH treatment, whereas HSC were unaffected by even 20 mM EtOH. These results suggest that NSC are much more sensitive to EtOH than HSC. Classic and novel PKC isozyme prote...