Contribution of Amyloid β-Peptides To Acrylamide-Induced Toxicity In Rat Brain Tissue

Acrylamide (ACR) is a well-known neurotoxic agent. The exact mechanism of neurotoxicity remains to be clarified. The following study aimed to evaluate the possible contribution of amyloid-β peptides to acrylamide-induced toxicity in rat brain tissue. Rats were randomly assigned to three groups, six rats in each group: control, low-dose (5mg/kg, i.p.) and high-dose (50 mg/kg, i.p.) acrylamide treated groups. In brain tissues, acetylcholinesterase activity (AChE) ,malondialdehyde (MDA), reduced glutathione (GSH), soluable amyloid β1-42 (Aβ1-42) peptide concentrations and also level of amyloid fibril formation (fibrillation) were analyzed. ACR treatment significantly reduced brain AChE activities in a dose-dependent manner (p<0.001). However, free Aβ1-42 concentrations and aggregation levels of amyloid fragments were significantly increased in brain tissues in low-dose-ACR treated group (p<0.01 and p<0.05 respectively). On the other hand, high-dose ACR treatment caused a significant decrease in tissue MDA and GSH levels (p<0.01). Our results have indicated that Aβ peptide-derived oxidative stress seemed to play a crucial role in ACR-induced neurotoxicity.