Vol. 9, Special Issue 1, Part J (2025)

Oxidative stress occurs when there is a disturbance in pro-oxidants and anti-oxidants. This balance is always very essential for maintaining homeostasis which when disturbed leads to many pathological conditions. This Oxidative stress is a ubiquitous cellular process leading to the Etiology of many illnesses. It has been recognized as a pathophysiologic mechanism underlying the development and progression of chronic kidney disease (CKD). Several endogenous mechanisms in the body are present to protect cells against oxidative stress. Glutathione contains a sulfhydryl (Thiol) containing synthesized and maintained at high concentrations in almost all cells and is one of the main mechanisms by which reactive oxygen species (ROS) are eliminated. N-acetylcysteine (NAC), a synthetic derivative of the endogenous amino acid L-cysteine and it is also a precursor of GSH. NAC is being used since years as a mucolytic and as an antidote to acetaminophen (Paracetamol) poisoning. Since NAC breaks the disulfide bonds of heavily cross-linked mucins, it therefore decreases mucus viscosity. N-acetylcysteine is very useful in both acute and chronic illness of kidney. NAC is shown to reduce kidney damage and CKD related morbidity. NAC increasingly became the epitome of an “antioxidant”. NAC is being widely used in both in experimental cell and animal biology, as well as clinical studies as an antioxidant. NAC acts by reducing disulfide bonds, by acting as a scavenger of reactive oxygen species and finally as a precursor for synthesis of glutathione. NAC uses are being applied, with a focus on respiratory diseases, acetaminophen poisoning, central nervous system disorders, cardiovascular disease, nephropathy and ophthalmology.