研究报告

  • 叶斌晖,周梦婷,黄黎明,蔡晨晨,寿晓璐,韩丽,贾秀英,张杭君.节球藻毒素对小鼠肝脏微结构的影响研究[J].环境科学学报,2013,33(1):304-311

  • 节球藻毒素对小鼠肝脏微结构的影响研究
  • Ultrastructure changes of mice liver induced by nodularin
  • 基金项目:杭州师范大学优秀中青年教师支持计划(No.JTAS2011-01-012)
  • 作者
  • 单位
  • 叶斌晖
  • 杭州师范大学环境科学系,杭州 310036
  • 周梦婷
  • 杭州师范大学环境科学系,杭州 310036
  • 黄黎明
  • 杭州师范大学环境科学系,杭州 310036
  • 蔡晨晨
  • 杭州师范大学环境科学系,杭州 310036
  • 寿晓璐
  • 杭州师范大学环境科学系,杭州 310036
  • 韩丽
  • 杭州师范大学环境科学系,杭州 310036
  • 贾秀英
  • 杭州师范大学环境科学系,杭州 310036
  • 张杭君
  • 杭州师范大学环境科学系,杭州 310036
  • 摘要:作为新型生物毒素,节球藻毒素(NOD)常见于爆发水华的水体中,是泡沫节球藻分泌的具有高肝毒性的次生代谢产物.由于其毒性高、暴露途径广且不易降解而日趋受到人们的重视.为了阐明NOD的肝毒性机理,本研究以模式生物小鼠为载体,研究亚慢性NOD诱导下小鼠肝脏在形态学、病理学上的微结构变化.结果表明,10 μg·kg-1·d-1 NOD下暴露21 d可诱导小鼠肝脏出现"草莓状表面"的肉眼可见的形态学改变.在H&E染色下,观察到在NOD暴露21 d可诱导小鼠肝脏出现微小结节、细胞嗜酸性病变、炎症细胞浸润、慢性淤胆及脂肪病变等病理学现象.当暴露时间延长到28 d时,嗜酸性病变恶化并出现嗜酸小体.在TEM观察下,小鼠肝细胞在NOD的诱导下出现肝细胞核皱缩、染色质凝集或边集、线粒体嵴横纹加深及分布散乱、内质网肿胀、核糖体脱粒等现象,并且在胞质中多有观察到微泡性脂肪变性及吞噬小泡.上述变化充分说明,在亚慢性暴露条件下,NOD依然具有强烈肝毒性.引起NOD慢性肝中毒的主要原因是肝细胞嗜酸性病变及炎症的诱发,并在暴露时间延长后进一步恶化,肝板结构破坏更加严重.
  • Abstract:As a new type of cyanobacterial toxins, Nodularin (NOD) is a kind of secondary metabolites produced by Nodularia spumigena with severe hepatotoxicity.Nod is always found in water bodies along with algae blooming.Increasing attentions are drawn for its high toxicity, wide exposure pathways to people and the difficulty of degradation.In order to clarify the mechanism of hepatotoxicity induced by NOD, mice were used as models to study the morphological and pathological changes in the livers under the subchronic exposure of NOD.Results showed that visible morphological change of "strawberry-like skin" was observed in mouse liver induced by NOD (10 μg·kg-1·d-1; i.p.) with 21 d.By H&E staining, under the exposure of NOD with 21 d, small nodules, acidophilic degeneration of cytoplasm, infiltration of inflammation cells, chronic cholestatic and steatosis were found.When the period was prolonged to 28 d, acidophilic degeneration was finally deteriorated to be the acidophilic body.Under the observation by TEM, pyknosis of hepatocytes, chromatic agglutination or margination, deepened mitochondria stripes along with chaotically distribution, endoplasmic reticulum swollen, and ribosomal threshing were occurred by the treatment of NOD, respectively.Moreover, lots of microvesicle steatosis and autophagy vesicle in cytoplasm of hepatocytes in the group treated with NOD were identified.According to the changes above, it is fully illustrated that NOD has high hepatotoxicity on mice under subchronic exposure.It is also suggested that acidophilic degeneration and the inducement of inflammation are the main reasons for hepatotoxicity of NOD.After the prolonged exposure periods, the hepatotoxicity may be further deteriorated and more serious damages to liver plate can be observed.

  • 摘要点击次数: 1772 全文下载次数: 2706