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These evidences support the notion that cancer cells could avoid oxidative stress-induced ferroptosis through activating the SIRT2-GCLC-GSH signaling axis

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These results indicated that trace Cu 2+ modified MOX-induced toxicity through coordinated transcriptional and metabolic regulation, thereby reshaped the oxidative stress response and physiological outcomes in C

MGL also improved intestinal barrier function by preserving tight junction proteins (ZO-1 and Claudin-1) and inhibiting intestinal epithelial cell apoptosis induced by TNBS and TNF- in mice and colon organoids