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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

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