motor neurone disease glutathione transferase transferases: substrates, inihibitors and pro-drugs in cancer and neurodegenerative diseases Evidence for alteration in the

It is believed to be due to autoimmune induced damage to the thyroid causing excess hormone release, and for this reason is not responsive to antithyroid drugs, KI or KCLO 4 , but does, if treatment is necessary, respond to prednisone(67)

Research published in the Journal of Clinical Medicine confirms glutathione's vital role in protecting cells from oxidative damage

*Correspondence: Shou-Dong Guo, [email protected] These authors have contributed equally to this work This article was submitted to Lipid and Fatty Acid Research, a section of the journal Frontiers in Physiology Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers

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Structured evidence overview Conclusions Strongest clinical signal: prevention of oxaliplatin-induced peripheral neuropathy, where IV GSH 1,500 mg/m2 before oxaliplatin reduces clinically significant neurotoxicity without compromising antitumor efficacy