![]() ![]() ![]() Subsequent studies suggested that administration even after 10 hours was partially effective and may also be beneficial in other, non-acetaminophen causes of acute liver failure, including drug induced liver injury. In multiple clinical trials, administration of acetylcysteine (also referred to as N-acetylcysteine or NAC) within 10 hours of an acetaminophen overdose effectively prevented serious liver injury. Restoration of glutathione stores ameliorates the cell injury from acetaminophen. ![]() Glutathione can become depleted in patients with malnutrition, chronic debilitating illnesses and chronic alcoholism, and becomes acutely depleted in patients with acetaminophen overdose leading to formation of toxic adducts of acetaminophen metabolites with essential intracellular molecules. Cysteine itself has a disagreeable odor and taste, while acetylated cysteine is more palatable and maintains the ability to support glutathione synthesis. Importantly, cysteine is required for synthesis of glutathione (a tripeptide of cysteine, glycine and glutamic acid) that is an essential intracellular antioxidant, providing protection against free radicals and other intracellular toxins including intermediates of drug metabolism. The amino acid cysteine has a thiol side chain that can undergo redox reactions and thus has antioxidant activity. Acetylcysteine (a seet" il sis' teen) is a modified amino acid that is used to reverse the toxic effects of acetaminophen overdose and prevent acute liver failure. ![]()
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