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Show 86 mechanism and they may be formed through aggregation of OAT with other While these proteins and oxidative adducts. results do not prove causal relationships, they allow speculation that early (within 24 h) alterations in OAT and VMAT2 contribute to the profound oxidative damage cause by METH. This initial damage leads to additional and numerous events, described previously, which cause prolonged oxidative stress and subsequent dopaminergic deficits. Attenuating the attenuate the initial damage and alterations in pathogenic cascade of METH-toxicity. understanding of METH-induced OAT and/or VMAT2 These findings aid in the persistent dopaminergic deficits mechanisms underlying OAT complex formation. may and the |