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Therefore, this study will focus specifically on analyzing alterations in redox homeostasis

Inhibition of glutaminolysis by Gln depletion, by chemical inhibition of the critical regulators of Gln metabolism such as GLS and MYC, or genetic knockdown of these genes and Gln transporters resulted in the inhibition of the essential CSC-driving signaling mechanisms (e.g., WNT/-catenin

this depletes cellular antioxidant defenses, resulting in uncontrolled lipid peroxidation and execution of ferroptosis (57,75)

S-adenosylmethionine in a feline acetominophen model of oxidative injury

Instead, they are cofactors for antioxidant enzymes