Abstract
Oxidative stress is a ubiquitous cellular process that results in damage to various biological molecules and it is involved in the etiopathogenesis of many diseases. The sulfhydryl-containing tripeptide glutathione (GSH), which is synthesized and maintained in high concentrations in all cells, is a component of one of the defense mechanisms. N-acetylcysteine, a synthetic derivative of the endogenous amino acid L-cysteine and a precursor of GSH, has been used for several decades as a mucolytic and antidote for acetaminophen (paracetamol) poisoning. As a mucolytic, N-acetylcysteine breaks the disulfide bonds of highly cross-linked mucins, thereby reducing the viscosity of the mucus. As an antidote for acetaminophen poisoning, N-acetylcysteine restores the hepatic GSH pool depleted during drug detoxification. More recently, enhance knowledge of N-acetylcysteine’s mechanisms of action has expanded its clinical use. This publication presents an overview of the most relevant and recent data on the clinical use of N-acetylcysteine in transplantology, neurology and ophthalmology.
Published Version
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