Mean to post this up a while ago. A couple have already been posted but here's a nice list of studies I found, focused on glutathione, but also some on Vit C, Selenium (required for glutathione enzymes) and Nrf2 (a whole topic in itself).
NAC = N-Acetyl-Cystine
(fyi there is a better cysteine pro-drug than NAC available now, and also an acylated form of glutathione)
http://www.ncbi.nlm.nih.gov/pubmed/3992009
Pretreatment with 100.0 mg/kg of ascorbic acid 30 minutes before each methamphetamine injection significantly (but not completely) attenuated this neurotoxic action of methamphetamine.
http://www.ncbi.nlm.nih.gov/pubmed/15199373
These results suggest that NAC could attenuate the reduction of DAT (dopamine transporter ) in the monkey striatum after repeated administration of MAP. Therefore, it is likely that NAC would be a suitable drug for treatment of neurotoxicity in dopaminergic nerve terminals related to chronic use of MAP in humans.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731235/?tool=pubmed
The idea that oxygen-based free radicals are involved in METH neurotoxicity is further strengthened by reports that the drug can reduce the levels of glutathione
http://www.ncbi.nlm.nih.gov/pubmed/9839724
Our observations provide further evidence in support of the oxidative stress hypothesis of MA neurotoxicity and indirectly suggest that drugs designed to increase glutathione might protect against such damage.
http://www.ncbi.nlm.nih.gov/pubmed/10642830
We have shown that dietary Selenium attenuated methamphetamine neurotoxicity and that this protection involves Glutathione Peroxidase-mediated antioxidant mechanisms
http://www.ncbi.nlm.nih.gov/pubmed/10650149
These data suggest that METH-induced neurotoxicity is mediated by the production of peroxynitrite, and selenium plays a protective role in METH-induced neurotoxicity.
http://www.ncbi.nlm.nih.gov/pubmed/10913590
These findings indicate selectivity of methamphetamine for the glutathione system and a role for methamphetamine in inducing oxidative stress.
http://www.ncbi.nlm.nih.gov/pubmed/12018843
METH toxicity seems to be produced by oxidative stress, as it was attenuated by the antioxidant glutathione
http://www.ncbi.nlm.nih.gov/pubmed/21882243
We found that Nrf2 deficiency exacerbated METH-induced damage to dopamine neurons
http://www.ncbi.nlm.nih.gov/pubmed/11746378
A dose-dependent depletion of total glutathione levels was detected in human brain microvascular endothelial cells exposed to METH
http://www.ncbi.nlm.nih.gov/pubmed/12230306
These results suggest that METH-induced disturbances in cellular redox status and that activation of AP-1 can play a critical role in signaling pathways leading to upregulation of inflammatory genes in vivo
http://www.ncbi.nlm.nih.gov/pubmed/15234256
These results suggest that NAC could prevent the behavioral changes (acute hyperlocomotion and development of behavioral sensitization) in rats and neurotoxicity in rat striatum after administration of MAP, and that NAC would be a useful drug for treatment of several symptoms associated with MAP abuse.
http://www.ncbi.nlm.nih.gov/pubmed/15111252
It was found that acute administration of methamphetamine (5 and 15 mg kg(-1)) resulted in production of oxidative stress as demonstrated by decreased glutathione and increased oxidized glutathione levels
http://www.ncbi.nlm.nih.gov/pubmed/16038959
Enantiomers of trans-phenylpropylene oxide (Pyrolytic products of smoked methamphetamine) were stereoselectively and regioselectively conjugated in a Phase II drug metabolism reaction catalyzed by human liver cytosolic enzymes consisting of conjugation with glutathione
http://www.ncbi.nlm.nih.gov/pubmed/16760923
The levels of the reduced form of glutathione (GSH) in striatum, amygdala, hippocampus and frontal cortex were significantly lower in METH-treated mice compared to control during the period of conditioned place preference training. Acute and repeated administration of NAC to METH-treated mice restored the decreased brain GSH but had no effect on controls.
http://www.ncbi.nlm.nih.gov/pubmed/22354084
This suggests that METH induces oxidative stress in various organs and that a combination of N-acetylcysteine amide as a neuro- or tissue-protective agent, in conjunction with current treatment, might effectively treat METH abusers.
http://www.ncbi.nlm.nih.gov/pubmed/17481858 Glutathione prevented dopamine-induced apoptosis of melanocytes and its signaling.
"Among various antioxidants used in this study, only thiol-containing antioxidants such as NAC or GSH inhibited both JNK and p38 MAPK activation and apoptosis, indicating the unique protective capacity of thiol compounds."