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Age, environmental toxins, poor diet, alcohol, and chronic illness can drain glutathione reserves faster than the body can replace them

The pharmacokinetic investigation determined that this compound is being hydrolyzed by the microbial colonies and metabolized in the mucosa of the intestine through phase II enzymes, submitted to methylation and conjugation process, forming methylated, glucuronic, and sulphated conjugates by the action of o-methyltransferase, UDP-glucosyltransferases, and sulfotransferases, respectively (Monteiro Espindola et al., 2019)

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Finally, we discuss several anti-ferroptosis therapeutic strategies spanning the use of radical trapping agents, iron modulation and glutathione dependent redox support and highlight the current landscape of clinical trials focusing on ferroptosis