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Acetylcysteine is a mucolytic agent which reduces the thickness of the mucus. Acetylcysteine is a ROS inhibitor[1].
Acetylcysteine prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. Acetylcysteine also prevents death of PC12 cells and sympathetic neurons[2]. Acetylcysteine causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells[3]. Acetylcysteine activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. Acetylcysteine protects neuronal cells from death evoked by withdrawal of trophic support. Acetylcysteine increases nitric oxide (NO) release from protein-bound stores in vascular tissue. Acetylcysteine pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it is suggested that Acetylcysteine interferes with redox-sensitive steps in the NGF mechanism[4].
Acetylcysteine (150, 300 mg/kg) treatment significantly reduces liver transaminases in all groups of treatment, mostly in group Acetylcysteine 300. Lung glutathione peroxidase is significantly increases in group Acetylcysteine 300 (P=0.04), while the other oxidation biomarkers show no significant differences[6]. Acetylcysteine improves cognition of 12-month-old SAMP8 mice in both the T-maze footshock avoidance paradigm and the lever press appetitive task without inducing non-specific effects on motor activity, motivation to avoid shock, or body weight[5].
Reference：
[1]. Halasi M, et al. ROS inhibitor N-acetyl-L-cysteine antagonizes the activity of proteasome inhibitors. Biochem J. 2013 Sep 1;454(2):201-8.
[2]. Ferrari G, et al. N-acetylcysteine (D- and L-stereoisomers) prevents apoptotic death of neuronal cells. J Neurosci. 1995 Apr;15(4):2857-66.
[3]. Tsai JC, et al. Induction of apoptosis by pyrrolidinedithiocarbamate and N-acetylcysteine in vascular smooth muscle cells. J Biol Chem. 1996 Feb 16;271(7):3667-70.
[4]. Yan CY, et al. Prevention of PC12 cell death by N-acetylcysteine requires activation of the Ras pathway. J Neurosci. 1998 Jun 1;18(11):4042-9.
[5]. Farr SA, et al. The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice. J Neurochem. 2003 Mar;84(5):1173-83.
[6]. Kalimeris K, et al. N-acetylcysteine ameliorates liver injury in a rat model of intestinal ischemia reperfusion. J Surg Res. 2016 Dec;206(2):263-272.
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