N-Acetylcysteine and Glutathione: Fortifying Antioxidant Defenses in the Aging Eye

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N-Acetylcysteine and Glutathione in the Aging EyeAge-related eye diseases – including glaucoma and retinal degeneration – are driven in part by oxidative stress, an imbalance between harmful free radicals (reactive oxygen species) and the eye’s antioxidant defenses. A key antioxidant in ocular tissues is glutathione (GSH), a tripeptide that scavenges free radicals and protects cells. N-acetylcysteine (NAC) is an acetylated form of the amino acid cysteine and serves as a precursor to glutathione. By delivering cysteine into cells, NAC can boost intracellular GSH production and indirectly quench oxidative damage () (). In retinal neurons and trabecular meshwork cells (the sponge-like tissue that regulates intraocular fluid outflow), elevating GSH may protect against damage caused by aging and high intraocular pressure. This article reviews how NAC, via bolstering glutathione, may fortify antioxidant defenses in the eye, what clinical evidence exists for visual benefits, and how ocular effects relate to NAC’s systemic redox and anti-inflammatory actions.NAC as a Glutathione Precursor in Retinal CellsNAC is a lipid-soluble cysteine source that crosses cell membranes and is quickly converted to cysteine, the rate-limiting building block for glutathione () (). Unlike cysteine alone, NAC can enter cells without specialized transporters. In neural tissues, higher cysteine enables more GSH synthesis. For example, retinal ganglion cells and Müller glia rely on glutamate–cysteine transporters to import cysteine and make GSH (). By supplementing NAC, cells bypass these transport steps, raising GSH levels inside neurons, photoreceptors, and supporting cells () ().Protection of Retinal Neurons and RPE In laboratory studies, NAC showed neuroprotective effects on the retina. In two mouse models of normal-tension glaucoma (glaucoma without high eye pressure), daily NAC prevented retinal ganglion cell (RGC) loss and vision decline in one model (EAAC1 knockout mice) by increasing retinal GSH and reducing oxidative stress () (). NAC suppresses oxidative damage and even dampens stress-induced autophagy in RGCs (). In the other model (GLAST knockout), NAC was less effective, suggesting that NAC’s benefit depends on which cells are primarily affected. This work highlights that in at least some glaucomatous optic neuropathies, NAC can raise glutathione in retinal neurons and protect them from degeneration () ().NAC also protects retinal pigment epithelium (RPE) and photoreceptors. In cultured human RPE cells, NAC blocked oxidative injury that models age-related macular degeneration (). In a clinical trial of patients with retinitis pigmentosa (an inherited retinal degeneration), oral NAC for several months improved cone photoreceptor function and slowed visual loss (). Specifically, a phase I trial found mean visual acuity (sharpness of central vision) improved modestly in subjects taking NAC, and the treatment was tolerable up to about 1,800 mg twice daily (). These findings suggest that in retinal degenerations driven by oxidative stress, boosting GSH with NAC can benefit retinal cells and vision.NAC and the Trabecular Meshwork Under Oxidative LoadThe trabecular meshwork (TM) is the tissue in the eye’s drainage angle that controls outflow of aqueous humor and thus influences intraocular pressure (IOP). TM cells are highly exposed to oxidative damage over a lifetime, and reduced antioxidant capacity in the TM is linked to glaucoma progre