AcetylcysteineS1623

N-acetylcysteine inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. N-acetylcysteine can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. N-acetylcysteine directly modifies the activity of several proteins by its reducing activity. ^[1] N-acetylcysteine prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. N-acetylcysteine also prevents death of PC12 cells and sympathetic neurons. ^[2] N-acetylcysteine causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells. ^[3] N-acetylcysteine activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. N-acetylcysteine protects neuronal cells from death evoked by withdrawal of trophic support. N-acetylcysteine increases nitric oxide (NO) release from protein-bound stores in vascular tissue. N-acetylcysteine pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it was suggested that NAC interferes with redox-sensitive steps in the NGF mechanism. ^[4]