N-acetyl L-cysteine attenuates oxidative damage and neurodegeneration in rat brain during aging.

N-acetyl-L-cysteine (NAC) is a precursor of cysteine which is known to increase the level of GSH in brain. Several neurodegenerative changes linked to oxidative stress take place in aging brain. This study is aimed to assess the neuroprotective effect of NAC supplementation on age- dependent neurodegeneration in the rat brain. Wistar rats: young (4 months) and old (24 months) age were supplemented with NAC (100 mg/kg b.w. orally) for 14 days. Enzymatic and non-enzymatic antioxidants such as SOD, catalase, GSH and total thiol (T-SH), prooxidants such as protein carbonyl (PC), advanced oxidation protein products (AOPP), reactive oxygen species (ROS) and malondialdehyde (MDA) were assessed in the brain homogenates. Furthermore, nitric oxide (NO), acetylcholinesterase activity (AChE), Na+/K+-ATPase activity and gene expression studies were also performed. The results indicate that NAC augmented the level of enzymatic and non enzymatic antioxidants with significant reduction in prooxidant levels in aged rats. NAC supplementation also downregulated the expression of inflammatory markers (TNF-α, IL-1β, IL-6), and upregulated the expression of marker genes associated with aging (Sirtuin-1) and neurodegeneration (NSE, NGB, Synapsin-I, MBP-2) in old rats. The present findings support a neuroprotective role of NAC which may provide its therapeutic implication in controlling age related neurological disorders.