| 慢性镉暴露对小鼠大脑皮质的毒性损伤作用 |
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| 引用本文： | 王莉,闻双全,贺双江,曹莹,邹辉,顾建红,刘学忠,卞建春,刘宗平,袁燕.慢性镉暴露对小鼠大脑皮质的毒性损伤作用[J].畜牧与兽医,2021(2):50-55. |
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| 作者姓名： | 王莉 闻双全 贺双江 曹莹 邹辉 顾建红 刘学忠 卞建春 刘宗平 袁燕 |
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| 作者单位： | 扬州大学兽医学院;江苏高校动物重要疫病与人兽共患病防控协同创新中心 |
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| 基金项目： | 国家自然科学基金项目(31772808);江苏高校优势学科建设工程项目(PAPD);扬州大学优秀青年骨干教师项目;扬州大学校教改课题(YZUJX2019-51C)。 |
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| 摘 要： | 为探究慢性镉暴露对小鼠大脑皮质的毒性损伤作用,选取雌性BALB/c小鼠用0(对照组)、5和25 mg/L不同浓度氯化镉自由饮水染毒16个月建立慢性镉中毒模型,试验结束后剖检采集小鼠完整脑组织,测定脑系数;光学显微镜和透射电子显微镜观察大脑皮质病理组织学和超微结构变化;比色法检测大脑皮质中总超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)的活性和还原型谷胱甘肽(GSH)、丙二醛(MDA)的含量。结果显示:与对照组相比,镉处理组脑系数均显著降低(P<0.05);镉处理组大脑皮质细胞核深染、固缩,呈三角形或不规则形,线粒体嵴断裂、溶解,部分呈空泡变性;镉处理组大脑皮质中T-SOD活力极显著下降(P<0.01),CAT活力显著下降(P<0.05),MDA、GSH含量极显著升高(P<0.01),5 mg/L氯化镉组GSH-PX活力显著升高(P<0.05),25 mg/L氯化镉组GSH-PX活力极显著升高(P<0.01)。提示:慢性镉暴露可影响小鼠脑发育,引起小鼠大脑皮质病理损伤、超微结构损伤和氧化损伤。
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| 关 键 词： | 镉 BALB/C小鼠 大脑皮质 病理损伤 超微结构损伤 氧化损伤 |
Toxic damage effect of chronic cadmium exposure on the cerebral cortex of mouse |
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| WANG Li,WEN Shuangquan,HE Shuangjiang,CAO Ying,ZOU Hui,GU Jianhong,LIU Xuezhong,BIAN Jianchun,LIU Zongping,YUAN Yan.Toxic damage effect of chronic cadmium exposure on the cerebral cortex of mouse[J].Animal Husbandry & Veterinary Medicine,2021(2):50-55. |
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| Authors: | WANG Li WEN Shuangquan HE Shuangjiang CAO Ying ZOU Hui GU Jianhong LIU Xuezhong BIAN Jianchun LIU Zongping YUAN Yan |
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| Institution: | (College of Veterinary Medicine,Yangzhou University,Yangzhou 225009,China;Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses,Yangzhou 225009,China) |
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| Abstract: | In order to explore the toxic damage effect of chronic cadmium exposure on the cerebral cortex of mice, female BALB/c mice were selected to be exposed to free drinking water with 0(the control group), 5 and 25(the experimental groups) mg/L different concentrations of cadmium chloride for 16 months to establish a chronic cadmium poisoning model. After the experiment, the whole brain tissues of the mice were dissected and samples were collected, and the brain coefficient was measured. The histopathological and ultrastructural changes in the cerebral cortex were observed using an optical microscope and a transmission electron microscope. Colorimetry was used to detect the activities of total superoxide dismutase(T-SOD), catalase(CAT), glutathione peroxidase(GSH-PX) and the contents of glutathione(GSH) and malondialdehyde(MDA) in the cerebral cortex. The results showed that, compared with the control group, the brain coefficient in the cadmium treatment groups reduced significantly(P<0.05);the nuclei were deeply stained and contracted, in triangular or irregular forms;and the mitochondrial cristae were broken and dissolved, and some of them were vacuolated in the cerebral cortex. The activity of T-SOD in the cerebral cortex decreased significantly(P<0.01), the activity of CAT decreased significantly(P<0.05), the content of MDA and GSH increased significantly(P<0.01), the activity of GSH-PX in the 5 mg/L cadmium chloride group increased significantly(P<0.05), and that in the 25 mg/L cadmium chloride group increased significantly(P<0.01). The present study suggested that chronic cadmium exposure might affect the brain development of mice and cause pathological damage,ultrastructural damage and oxidative damage in the cerebral cortex of mice. |
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| Keywords: | cadmium BALB/c mice cerebral cortex pathological damage ultrastructural damage oxidative damage |
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