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doi: 10.1016/j.cocis.2008.01.002 197

Although the pathophysiological mechanisms of DPN are not entirely understood, certain pathways have been identified in preclinical studies driving harmful metabolic processes

Treating cells with L-buthionine sulfoximine (BSO), an inhibitor that blocks the synthesis of GSH, renders neuronal SH-SY5Y cells expressing mutant valosin-containing protein (VCP) R487H more susceptible to oxidative stress (Hirano et al., 2015) and increases mutant SOD1 toxicity (Alvarez-Zaldiernas et al., Drosophila models increases markers of oxidative stress, including protein carbonylation and glutathione S transferase D1 (Duan et al., 2010