二硫化碳对大鼠神经组织氧化-抗氧化系统的影响

目的探讨二硫化碳亚慢性染毒对大鼠神经组织氧化-抗氧化系统的影响。方法雄性Wistar大鼠30只，随机分为对照组和低、高剂量染毒组，每组10只。利用300和500mg·k^-1·d^-1二硫化碳灌胃染毒，每周5次，连续12周，建立大鼠中毒性神经病模型，测定大鼠大脑、脊髓和坐骨神经中丙二醛（MDA）、活性氧（ROS）、谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSHPx）、过氧化氢酶（CAT）和总抗氧化能力（T-AOC）等指标的变化。结果与对照组相比，染毒大鼠神经组织中MDA和ROS含量明显增加。其中，低、高剂量组大脑MDA含量分别增加20．7％、33．6％，脊髓MDA含量增加18．5％、23.3％，坐骨神经MDA含量增加23.1％、53．0％；低、高剂量组大脑ROS含量分别升高20．1％、34．9％，高剂量组脊髓、坐骨神经ROS含量分别升高14．1％、15．4％，差异均有统计学意义（P〈0．05或P〈0，01）。与对照组相比，染毒大鼠神经组织中GSH含量、SOD、GSH—Px、CAT活力和T—AOC明显降低，其中，低、高剂量组大脑GSH含量分别降低17．2％、26，5％，脊髓GSH含量降低26．4％、31．2％，坐骨神经GSH含量降低15．1％、20．0％；低、高剂量组大脑T—AOC分别降低11．1％、26．4％，脊髓T．AOC降低15．1％、38．4％，坐骨神经T—AOC降低35．6％、42．3％；低、高剂量组脊髓SOD活力分别降低12．1％、25．4％，坐骨神经SOD活力降低16．4％、30-3％；低、高剂量组脊髓GSH—Px活力分别降低17．3％、32．5％，坐骨神经GSH．Px活力降低17．1％、21．5％；高剂量组大脑GSH—Px、SOD活力分别降低12．6％、30．1％；低、高剂量组大脑CAT活力分别降低17．5％、39．4％，脊髓CAT活力降低25．2％、31．3％，坐骨神经CAT活力降低17．1％、36．9％，上述差异均有统计学意义（P〈0．05或P〈0．01）。结论二硫化碳损伤了大鼠神经组织的氧化-抗氧化系统，可能与二硫化碳中毒性神经病的发生机制有关。

Effect of carbon disulfide on oxidation-antioxidation function of rat nerve tissues

OBJECTIVE: To investigate the effect of carbon disulfide (CS(2)) on oxidation-antioxidation function of rat nerve tissues. METHODS: Thirty male Wistar rats were randomly divided into the control group, the low-dosage exposure group and the high-dosage group, 10 rats each. The rats of the two exposure groups were administered with CS(2) by gavage at a dosage of 300 or 500 mgxkg(-1)xd(-1), 5 times every week for continuous 12 weeks. The alterations in glutathione (GSH), malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), hydrogen peroxidase (CAT) and total anti-oxidation (T-AOC) in cerebrum, spinal cord, and sciatic nerve of CS(2)-treated animals were assayed. RESULTS: The results showed that the contents of MDA and ROS in nerve tissues of CS(2)-treated groups increased significantly except ROS in spinal cord and sciatic nerve of low dose group. The content of MDA was increased by 20.7% and 33.6% respectively in the cerebrum of the rats of the low-dosage group and the high-dosage group, by 18.5% and 23.3% respectively in the spinal cord, and by 20.7% and 53.0% respectively in the sciatic nerve, The content of MOS was increased by 20.1% and 34.9% respectively in the cerebrum of the rats of the low-dosage group and the high-dosage group, and by 14.1% and 15.4% respectively in the spinal cord and the sciatic nerve of the rats of the high-dosage group (P < 0.05 or P < 0.01). Furthermore, the activities of SOD, GSH-Px, CAT and T-AOC decreased significantly except GSH-Px and SOD in cerebrum of low dose group. The content of GSH was decreased by 17.2% and 26.5% respectively in the cerebrum of the rats of the low-dosage group and the high-dosage group, by 26.4% and 31.2% respectively in the spinal cord, and by 15.1% and 20.0% respectively in the sciatic nerve. The content of T-AOC was decreased by 11.1 and 26.4% respectively in the cerebrum of the rats of the low-dosage group and the high-dosage group, by 15.1% and 38.4% respectively in the spinal cord, and by 35.6% and 42.3% respectively in the sciatic nerve. The activity of SOD was decreased by 12.1% and 25.4% respectively in the spinal cord of the rats of the low-dosage group and the high-dosage group and by 16.4% and 30.3% respectively in the sciatic nerve. The activity of GSH-Px was decreased by 17.3% and 32.5% respectively in the spinal cord of the rats of the low-dosage group and the high-dosage group and by 17.1% and 21.5% respectively in the sciatic nerve. The activity of GSH-Px and SOD was decreased by 12.6% and 30.1% respectively in the cerebrum of the rats of the high-dosage group. The activity of CAT was decreased by 17.5% and 39.4% respectively in the cerebrum of the rats of the low-dosage group and the high-dosage group, by 25.2% and 31.3% respectively in the spinal cord, and by 17.1% and 36.9% respectively in the sciatic nerve (P < 0.05 or P < 0.01). CONCLUSION: Subchronic exposure to CS(2) can induce significant changes of oxidation-antioxidation function in rat nerve tissues, which might be related to CS(2)-induced neurotoxicity.