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Results Neuronal GCLC knockout leads to brain atrophy accompanied by neuronal cell death To examine how the declines in GCLC and glutathione might affect brain homeostasis, we prepared GCLC floxed X CaMKII-Cre (GCLC-KO) mice whose GCLC expression is deleted in calcium/calmodulin-dependent protein kinase II (CaMKII)-positive neurons

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Finally, SF treatment resulted in a 5.4-fold increase in basal and high glucose in sulfiredoxin (SRXN1) involved in reducing the cysteine-sulfinic acid formed under exposure to oxidants [43]