Protective Effects of N Acetylcysteine and Vitamin E against Acrylamide-induced Neurotoxicity in Rats

When many widely ingested foods are heated, a toxin called acrylamide (ACR) is created. The aim of our research was to investigate if N acetylcysteine (NAC) and/or vitamin E (Vit E) could provide protection against neurotoxicity induced by ACR. Rats were classified into seven groups of 7 rats; control (saline); NAC (150 mg/kg bw); Vit E (100 mg/kg bw); ACR (20 mg/kg bw orally); ACR+NAC; ACR+Vit E; ACR+NAC+Vit E. Saline, NAC and/or Vit E were administered orally, once daily for 30 days. Acetylcholinesterase (AChE) inhibition, glutathione depletion, and elevated levels of malondialdehyde (MDA), were all observed after ACR intoxication. Furthermore, ACR diminished superoxide dismutase (SOD) and catalase (CAT) activities, as well as inflammatory mediators as interleukins (IL-1, IL-6), and tumor necrosis factor-& alpha; (TNF-& alpha;). The combined treatment of ACR with NAC or Vit E dramatically reduced both oxidative and biochemical consequences, with a more frequent return to normal values. To conclude, NAC or Vit E supplementation may alleviate ACR-induced neuronal injury, most likely due to NAC or Vit E antioxidant, anti-inflammatory, and anti-apoptotic effects.

Automated summary

The aim was to investigate the protective effects of N-acetylcysteine (NAC) and/or vitamin E (Vit E) against acrylamide (ACR)-induced neurotoxicity. Rats were classified into different groups and treated with either NAC or Vit E alone or in combination with ACR. ACR ingestion resulted in various effects, including inhibition of acetylcholinesterase (AChE), depletion of glutathione, increased malondialdehyde (MDA) levels, and decreased activities of superoxide dismutase (SOD) and catalase (CAT). NAC or Vit E supplementation significantly reduced these adverse effects.