二硫化碳对大鼠神经组织氧化-抗氧化系统的影响

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

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 effect of carbon disulfide （CS2） 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 CS2 by gavage at a dosage of 300 or 500mg·k^-1·d^-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 CS2-treated animals were assayed. Results The results showed that the contents of MDA and ROS in nerve tissues of CS2-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 lowdosage 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 ofT 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 ofGSH 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〈O.05 or P〈 0.01）. Conclusion Subchronic exposure to CS2 can induce significant changes of oxidation-antioxidation function in rat nerve tissues, which might be related to CS2-induced neurotoxicity.