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Multiple animal model and cell culture studies have shown a compensatory upregulation of GSH in response to oxidative stress (Ong et al., 2000), including exposure to toxins such as mercury (Hoffman et al., 2005), radiation (Di Toro et al., 2007), neonatal alcohol (Smith et al., 2005), and methamphetamine (Harold et al., 2000), as well as neurological diseases such as models of Parkinsons disease (Aluf et al., 2010

The activation of glial cells was observed in similar regions to those where neuronal loss and atrophy were severe, i.e