of Mcl-1S did not show any significant impact on cellular viability and apoptosis in control-untreated cells. These results suggest that EtOH-mediated toxicity may not be associated with increased copies of Mcl-1S isoform, but may be related to the decreased copies of Mcl-1L in neural progenitor cells. In order to determine specificity of Mcl-1L in rescue of cytotoxicity induced by EtOH, possible impact of Bcl-2, a key member of BCL2 family genes, was also assessed (Fig. 7b). Neural progenitor cells were transfected with increasing concentrations of a mammalian expression vector encoding human Bcl-2 and either exposed to 50 mM EtOH for 24 h or left untreated. Cell viability was analyzed by MTT cell viability assay. The results suggest that unlike Mcl-1L, Bcl-2 overexpression had no significant rescue of viability loss induced by EtOH, suggesting a unique and specific role of Mcl-1 gene in EtOH-mediated cytotoxicity in neural progenitors.
