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Cellular defense mechanisms, primarily involving the SOD, CAT, and GSH, counteract ROS-mediated damage

TNF secreted from adipose tissue can induce hepatocyte apoptosis and exacerbate inflammation through activation of the NF-B and JNK pathways, among other pathways [217, 218]

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In addition, the increased flux through CYSTGL not only channels the metabolites toward glutathione synthesis but also produces ammonia as an obligatory byproduct, representing a metabolic trade-off between redox homeostasis maintenance and toxic byproduct generation