[A study of neurotoxicity of crotonaldehyde in male rats]

Objective: To investigate the neurotoxicity of crotonaldehyde exposure in male rats and its possible mechanism of action. Methods: From July to October 2019, 24 specific pathogen-free male Wistar rats were randomly divided into control group and 2.5, 4.5, and 8.5 mg/kg exposure groups, with 6 rats in each group, and the rats in these groups were given oral administration of crotonaldehyde solution at doses of 0.0, 2.5, 4.5, and 8.5 mg/kg, respectively, 5 times a week for 90 consecutive days. Body weight was measured after exposure, and brain tissue and liver tissue were collected. The activity of acetylcholinesterase (AChE) in brain tissue and the level of acetylcholine (ACh) in liver tissue were measured; The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the levels of malondialdehyde (MDA) and reduced glutathione (GSH) in brain tissue were measured; ELISA was used to measure the levels of interleukin-6 (IL-6) , interleukin-1β (IL-1β) , and tumor necrosis factor-α (TNF-α) in brain tissue. Results: Compared with the control group, the 2.5, 4.5, and 8.5 mg/kg exposure groups had a significant reduction in the activity of AChE in brain tissue, and the 8.5 mg/kg exposure group had a significant increase in the level of ACh in liver tissue (P<0.05) . Compared with the control group, the 4.5 and 8.5 mg/kg exposure groups had a significant increase in the level of MDA and significant reductions in the level of GSH and the activities of SOD and GSH-Px in brain tissue (P<0.05) . Compared with the control group, the 2.5, 4.5, and 8.5 mg/kg exposure groups had significant increases in the levels of TNF-α and IL-6 in brain tissue, and the 4.5 and 8.5 mg/kg exposure groups had a significant increase in the level of IL-1β (P<0.05) . Conclusion: Crotonaldehyde exposure can induce nervous system injury in rats, possibly by altering oxidative balance and upregulating the expression of inflammatory factors in brain tissue.