Acetylcysteine (N-acetylcysteine)

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]

N-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]

• Cell lines

  MCF cells

• Concentrations

  5 mM

• Incubation Time

  24 h

• Method

  Cells were treated with indicated concentration of drug for 24 h.

• Animal Models

  Male SAMP8 mice

• Dosages

  100 mg/kg

• Administration

  s.c.