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二硫化碳对大鼠视网膜组织诱导型一氧化氮合酶及细胞凋亡的影响
引用本文:王军明,张虹,丁爱东,杨红.二硫化碳对大鼠视网膜组织诱导型一氧化氮合酶及细胞凋亡的影响[J].中华劳动卫生职业病杂志,2007,25(5):271-274.
作者姓名:王军明  张虹  丁爱东  杨红
作者单位:1. 430030,武汉,华中科技大学同济医学院附属同济医院眼科
2. 内蒙古自治区临河市医院眼科
摘    要:目的探讨二硫化碳(CS2)对大鼠视网膜组织诱导型一氧化氮合酶(iNOS)及细胞凋亡的影响。方法将24只SD雄性大鼠随机分为对照组、低剂量CS2染毒组和高剂量CS2染毒组,染毒结束后取视网膜组织制成切片,测量内视网膜厚度比率,还原型烟酰胺腺嘌呤二核苷酸黄递酶染色(NADPH-NDP)法检测iNOS活力,原位缺口末端标记法(TUNEL)检测细胞凋亡。结果(1)染毒组的内视网膜(包括内核层、内丛状层、节细胞层、神经纤维层和内界膜)厚度减小,与对照组相比,差异有统计学意义(P〈0.05);高剂量染毒组与低剂量染毒组之间差异亦有统计学意义(P〈0.05)。(2)染毒组视网膜iNOS表达增加,与对照组相比,差异有统计学意义(P〈0.05或P〈0.01);高剂量染毒组与低剂量染毒组之间差异亦有统计学意义(P〈0.05)。(3)染毒组视网膜出现细胞凋亡,凋亡指数与对照组相比,差异有统计学意义(P〈0.05或P〈0.01);高剂量染毒组与低剂量染毒组之间差异亦有统计学意义(P〈0.05)。结论CS2能激活视网膜组织iNOS表达,由此产生的过量的NO可损伤视网膜细胞。同时,视网膜细胞凋亡也是CS2所致视网膜损害的机制之一。

关 键 词:二硫化碳  视网膜  一氧化氮合酶  细胞凋亡
修稿时间:2006-11-20

Effect of carbon disulfide on inducible nitric oxide synthase and apoptosis in retina of rats
WANG Jun-ming,ZHANG Hong,DING Ai-dong,YANG Hong.Effect of carbon disulfide on inducible nitric oxide synthase and apoptosis in retina of rats[J].Chinese Journal of Industrial Hygiene and Occupational Diseases,2007,25(5):271-274.
Authors:WANG Jun-ming  ZHANG Hong  DING Ai-dong  YANG Hong
Institution:Department of Ophthalmology , Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Abstract:OBJECTIVE: To investigate the effect of carbon disulfide (CS2) on inducible nitric oxide synthase (iNOS) and apoptosis in in the retina of rats. METHODS: Twenty-four male SD rats were randomly divided into 3 groups the control group, the group receiving high-dose CS2 and the group receiving low-dose CS2. After treatment, retina were harvested and made into slice. The thickness of inner retina including outer plexiform layer, inner nuclear layer, ganglion cell layer, optic nerve fiber and inner limiting membrance was measured. Expression of iNOS in retina was measured by NADPH-NDP histochemical assay. Apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). RESULTS: (1) The thickness of inner retina decreased in groups receiving CS2. There was significant difference between control group and groups receiving CS2 (P < 0.05). There was also significant difference between group receiving high-dose CS2 and group receiving low-dose CS2 (P < 0.05). (2) The expression of iNOS increased in groups receiving CS2. There was significant difference between control group and groups receiving CS2 (P < 0.05 or P < 0.01). There was also significant difference between the group receiving high-dose CS2 and the group receiving low-dose CS2 (P < 0.05). (3) Apoptosis was observed in groups receiving CS2. There were significant differences in apoptosis index between the control group and groups receiving CS2 (P < 0.05 or P < 0.01). There was also significant difference between the group receiving high-dose CS2 and the group receiving low-dose CS2 (P < 0.05). CONCLUSIONS: CS2 can evoke the expression of iNOS, and the nitric oxide thus produced can be one of the causes of retina destruction. And apoptosis is also one of the causes of retina destruction.
Keywords:Carbon disulfide  Retina  Nitric oxide synthase  Apoptosis
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