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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: Alcohol Clin Exp Res. 2008 Aug 20;32(11):1884–1892. doi: 10.1111/j.1530-0277.2008.00769.x

Fig. 6. PARP-1 -related events in response to ethanol exposure.

Fig. 6

Within minutes of ethanol exposure, there is an enhanced expression of reactive oxygen species (ROS) in cultured fetal rat cerebral cortical neurons (Heaton et al., 2003; Kotch et al., 1995; Maffi et al., 2008; Ramachandran et al., 2001, 2003). This scheme presents the concept that PARP-1 is activated secondary to DNA damage, ultimately leading to PARylation of nuclear proteins. Within 2 hours of ethanol exposure there is an observable increase in translocation of AIF to the nuclear compartment, an event that may be mediated by PARP-1. Within 12 hours of ethanol treatment, there is caspase-3 -mediated inactivation of PARP-1. However, the DNA fragmentation process has already commenced in select neurons, in response to nuclear accumulation of AIF.