A plastic stabilizer dibutyltin dilaurate induces subchronic neurotoxicity in rats  

作　　者：Minghua Jin Peilin Song Na Li Xuejun Li Jiajun Chen 

机构地区：[1]Department of Health Laboratory Technology, College of Public Health of Jilin University, Changchun 130021, Jilin Province, China [2]Department of Infection, Central Hospital of Siping, Siping 136000, Jilin Province, China [3]Department of Otorhinolaryngology, Jilin Provincial People's Hospital, Changchun 130021, Jilin Province, China [4]Department of Neurology, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin Province, China

出　　处：《Neural Regeneration Research》2012年第28期2213-2220,共8页中国神经再生研究（英文版）

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.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.

关 键 词：dibutyltin dilaurate oxidative damage cell cycle apoptosis ULTRASTRUCTURE DNA damage braininjury sub-chronic poisoning 

分 类 号：Q959.837[生物学—动物学] TQ433.432[化学工程]