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However, after cellular GSH depletion it is thought that NAPQI causes cytotoxicity by binding to cellular macromolecules, although the exact mechanism of cellular toxicity remains a subject of controversy [11] [12]

Glutamine deficiency in extracellular fluid exerts adverse effects on protein and amino acid metabolism in skeletal muscle of healthy, laparotomized, and septic rats

It is initiated through two principal pathways: the extrinsic (death receptor-mediated) and intrinsic (mitochondrial) pathways, which converge on the activation of executioner caspases (Fig

Bioorg Chem 128:106101

Redox status is altered in G6PD deficient RBCs, supporting the idea that G6PD deficiency confers protection against malarial infection (although predisposes to hemolysis)