Herein, by qualitative and quantitative analysis, we report that alcohol exposure selectively induces a shift in Mcl-1L/Mcl-1S ratio in neural progenitors and immature neurons but not in mature neuron cultures. Interestingly, the reduction in Mcl-1L and increase in Mcl-1S isoforms correlates with viability loss and cell death due to the apoptosis activation in neural progenitors. Furthermore, ectopic expression of Mcl-1L isoform is able to recover toxicity induced by EtOH suggesting a novel role of Mcl-1L isoform in neurotoxicity associated with EtOH exposure.
