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In contrast, mutation of the C-terminal active site cysteine increases the activity of GLRX, presumably by preventing disulfide bond formation between the two active site cysteines 20,21 , and renders GLRX a monothiol enzyme only capable of catalysis of (de)glutathionylation 22

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Animals received a single intravenous (IV) injection (0.2 mL) of Co-60 solution at 7.2 0.5 KBq dose in sterile saline via an indwelling jugular vein cannula

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Remarkably, inhibition of ferroptosis by Lip-1 reduces GIC incidence in DEX-injected rat models