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Conclusions Our novel data manifested that GPX3, which was capable of inducing apoptosis via AMPK/ERK1/2 pathway and antagonizing autophagy-related ferroptosis through AMPK/m-TOR signalling, was a promising therapeutic target for BPH in the future

We also assessed whether the rate of weight regain varied depending on the type of treatment provided during the follow-up period with no treatment, comparing behavioural support with no support and active treatment (behavioural support or metformin) with non-active treatment (placebo or nothing)

Hepatocytes serve as the primary site of INH bioactivation, where the drug is metabolized by catalase-peroxidase and cytochrome P450 2E1 into reactive metabolites (hydrazine, acetylhydrazine) and ROS ( 3.6 INH-OS: dose-dependent SOD/GPx/CAT suppression impairs RBC ROS/lipid peroxide clearance INH treatment caused significant dysregulation of genes associated with OS in the human hepatoma HepG2 cell line (Figures 13)

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Lee HJ, Ju J, Paul S, So JY, DeCastro A, Smolarek A, et al