A plastic stabilizer dibutyltin dilaurate induces subchronic neurotoxicity in rats

摘要

Dibutyltin dilaurate functions as a stabilizer for polyvinyl chloride. In this study, experimental rats were intragastrically administered 5, 10, or 20 mg/kg dibutyltin dilaurate to model sub-chronic poisoning. After exposure, our results showed the activities of superoxide dismutase and glutathione peroxidase decreased in rat brain tissue, while the malondialdehyde and nitric oxide content, as well as nitric oxide synthase activity in rat brain tissue increased. The cell cycle in the right parietal cortex was disordered and the rate of apoptosis increased. DNA damage was aggravated in the cerebral cortex, and the ultrastructure of the right parietal cortex tissues was altered. The above changes became more apparent with exposure to increasing doses of dibutyltin dilaurate. Our experimental findings confirmed the neurotoxicity of dibutyltin dilaurate in rat brain tissues, and demonstrated that the poisoning was dose-dependent. Research Highlights (1) After dibutyltin dilaurate sub-chronic poisoning, the activities of superoxide dismutase and glutathione peroxidase in rat brain tissue decreased, while the malondialdehyde, nitric oxide content and nitric oxide synthase activity increased. (2) After dibutyltin dilaurate sub-chronic poisoning, the percentage of cells at G ₀ /G ₁ phase in rat brain tissue increased, while that of cells at S phase and G ₂ +M phase decreased. Also, the apoptotic rate of brain cells increased, and DNA damage was aggravated. (3) 20 mg/kg dibutyltin dilaurate exposure resulted in apparent neuropil cavitation in rat brains, as shown by cavitation and other ultrastructural changes, with glial filaments dissolving within the axon.