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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500 mg·kg~(-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(GSH- Px)、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。
Objective To investigate the effects of sub-chronic exposure to carbon disulfide on the oxidation and anti-oxidative system of nerve tissue in rats. Methods Thirty male Wistar rats were randomly divided into control group and low and high dose exposure groups, 10 rats in each group. Rats were challenged with 300 and 500 mg · kg -1 d -1 of carbon disulfide for 5 weeks. The rats were sacrificed for 12 consecutive weeks. The rat model of neurotoxicity was established. The brain, spinal cord and sciatic nerve (MDA), reactive oxygen species (ROS), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH- Px), catalase CAT) and total antioxidant capacity (T-AOC) and other indicators of change. Results Compared with the control group, the content of MDA and ROS in the nerve tissue of the exposed rats increased significantly. The content of MDA in brain increased by 20.7% and 33.6%, the content of MDA in spinal cord increased by 18.5% and 23.3%, the content of MDA in sciatic nerve increased by 23.1% and 53.0% respectively. The content of ROS in brain increased by 20.1% and 20.1% %, 34.9%. The content of ROS in the spinal cord and sciatic nerve in the high dose group increased by 14.1% and 15.4%, respectively, with statistical significance (P <0.05 or P <0.01). Compared with the control group, GSH content, SOD, GSH-Px, CAT activity and T-AOC in the nerve tissue of the treated rats were significantly decreased, and the contents of GSH in the low and high dose groups decreased by 17.2% and 26.5% The contents of GSH and GSH in the sciatic nerve decreased by 26.4% and 31.2%, 15.1% and 20.0% respectively. The brain T-AOC in the low and high dose groups decreased by 11.1% and 26.4% AOC decreased 35.6% and 42.3% respectively. The activity of SOD in the spinal cord decreased by 12.1% and 25.4% in the low and high dose groups, while decreased 16.4% and 30.3% in the sciatic nerve. The GSH-Px activity in the spinal cord decreased by 17.3% and 32.5% The activities of GSH-Px and SOD decreased by 12.6% and 30.1% in the high dose group, and decreased by 17.5% and 39.4% in the low and high dose groups respectively. The spinal cord CAT The vitality decreased by 25.2% and 31.3%, and the CAT activity of sciatic nerve decreased by 17.1% and 36.9%, respectively. All these differences were statistically significant (P <0.05 or P <0.01). Conclusion Carbon disulfide (SC) injured the oxidative-antioxidant system in rat nerve tissue and may be related to the pathogenesis of carbon disulfide poisoning neuropathy.