| 沈文静,张潇,赵子昂,方再光,谢曦,王蓉,胡文婷.敌草快对斑马鱼组织损伤及慢性肝脏损害作用[J].农业环境科学学报,2021,40(5):949-956. |
| 敌草快对斑马鱼组织损伤及慢性肝脏损害作用 |
| Histological changes and chronic liver injury of diquat in zebrafish(Brachydanio rerio) |
| 投稿时间：2021-01-13 |
| DOI：10.11654/jaes.2021-0043 |
| 中文关键词: 敌草快 斑马鱼 组织结构 肝脏损害 |
| 英文关键词: diquat zebrafish histopathology liver injury |
| 基金项目:国家自然科学基金青年基金项目（31902418）；海南省自然科学基金青年基金项目（319QN160）；海南大学科研启动基金项目（KYQD（ZR）19108） |
| 作者 | 单位 | E-mail | | 沈文静 | 海南大学生命科学与药学院, 热带生物资源教育部重点实验室, 海口 570228 | | | 张潇 | 海南大学生命科学与药学院, 热带生物资源教育部重点实验室, 海口 570228 | | | 赵子昂 | 海南大学生命科学与药学院, 热带生物资源教育部重点实验室, 海口 570228 | | | 方再光 | 海南大学海洋学院, 海口 570228 | | | 谢曦 | 海南大学生命科学与药学院, 热带生物资源教育部重点实验室, 海口 570228 | | | 王蓉 | 海南大学生命科学与药学院, 热带生物资源教育部重点实验室, 海口 570228 | | | 胡文婷 | 海南大学生命科学与药学院, 热带生物资源教育部重点实验室, 海口 570228 | huwt_0@hainu.edu.cn |
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| 中文摘要: |
| 探讨敌草快对斑马鱼（Brachydanio rerio）的毒性效应及其致毒机理。观察敌草快对斑马鱼鳃和肝脏组织的急性损伤效应，并分析慢性敌草快胁迫对斑马鱼肝脏超氧化物歧化酶（SOD）、谷胱甘肽-S转移酶（GST）、丙二醛（MDA）和甘油三酯（TG）的影响。敌草快对斑马鱼的96 h半致死浓度（LC50）为16.92 mg·L-1；斑马鱼暴露于8.46、4.23、1.69 mg·L-1敌草快中96 h后，苏木精-伊红（H-E）染色显示鳃小片出现卷曲变形、上皮细胞排列不规则和细胞脱落现象，肝细胞呈现明显的肿大，胞质产生空泡化，局部区域细胞坏死、溶解，斑马鱼鳃和肝脏组织的损伤程度随着敌草快浓度的增加而加重；暴露于1.69、0.84 mg·L-1和0.34 mg·L-1敌草快中28 d后，斑马鱼肝脏的SOD活性变化表现为降-升-降，并呈现出剂量效应；1.69 mg·L-1和0.84 mg·L-1敌草快处理组肝脏的GST活性表现为先升后降，28 d时显著低于对照组（P<0.01），0.34 mg·L-1敌草快处理组肝脏的GST活性无显著变化（P>0.05）；与对照组相比，处理组肝脏的MDA含量在第7 d和14 d变化均不明显（P>0.05），在第28 d时0.84 mg·L-1和1.69 mg·L-1敌草快处理组肝脏的MDA含量极显著升高（P<0.01）；处理组斑马鱼肝脏中TG的含量均从14 d开始出现增加。水体中的敌草快对斑马鱼有较严重的急性损伤作用，长时间暴露于低浓度敌草快中的斑马鱼，其肝脏会发生氧化应激反应，肝脏代谢功能也会受到影响。 |
| 英文摘要: |
| This study investigated the toxic effect and mechanism of diquat intoxication on zebrafish(Brachydanio rerio). The acute damage of diquat on the morphology of gill and liver in zebrafish were observed, and the chronic influences on the activity of superoxide dismutase (SOD) and glutathione transferase(GST), malondialdehyde(MDA) content, and triglyceride(TG) in the liver were analyzed. The 96-h LC50 of diquat to zebrafish was 16.92 mg·L-1. After acute exposure to 1.69, 0.84 mg·L-1, and 0.34 mg·L-1 of diquat for 96 h, the results of hematoxylin and eosin(H-E) staining showed that the gill fragments were curled and shortened, and epithelial cell suffered from edema, deformation, and necrosis. Hepatocytes showed evident enlargement, and local necrosis and the dissolution of hepatocytes and vacuolation of cytoplasm were observed. The pathological changes in the gills and liver of zebrafish were aggravated with the increase in diquat concentration. Zebrafish were exposed to 1.69, 0.84 mg·L-1, and 0.34 mg·L-1 of diquat for 28 days. The SOD activity in the liver of zebrafish in each group decreased first, then increased, and then gradually decreased, and a certain concentration -effect relationship was observed. The GST activity in the liver of zebrafish first increased and then decreased being induced by 1.69 mg·L-1 and 0.84 mg·L-1 diquat, followed by a significant decrease on the 28th day(P<0.05). There was no significant change in 0.34 mg·L-1 diquat during the exposure(P>0.05). The MDA content in the liver of zebrafish in each group did not change significantly on the 7th and 14th day(P>0.05). On 28th day, the MDA contents treated with 0.84 mg·L-1 and 1.69 mg·L-1 diquat increased significantly(P<0.01). The TG content in the liver of zebrafish with diquat exposure increased from the 14th day in each treatment group. The results indicate that diquat causes severe acute damage to zebrafish, and long-term exposure could cause oxidative stress in liver and may affect liver metabolism. |
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