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| Histological changes and chronic liver injury of diquat in zebrafish(Brachydanio rerio) |
| Received:January 13, 2021 |
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| KeyWord:diquat;zebrafish;histopathology;liver injury |
| Author Name | Affiliation | E-mail | | SHEN Wen-jing | Key Laboratory of Tropical Biological Resources, Ministry of Education, School of Life Science and Pharmacy, Hainan University, Haikou 570228, China | | | ZHANG Xiao | Key Laboratory of Tropical Biological Resources, Ministry of Education, School of Life Science and Pharmacy, Hainan University, Haikou 570228, China | | | ZHAO Zi-ang | Key Laboratory of Tropical Biological Resources, Ministry of Education, School of Life Science and Pharmacy, Hainan University, Haikou 570228, China | | | FANG Zai-guang | College of Oceanology, Hainan University, Haikou 570228, China | | | XIE Xi | Key Laboratory of Tropical Biological Resources, Ministry of Education, School of Life Science and Pharmacy, Hainan University, Haikou 570228, China | | | WANG Rong | Key Laboratory of Tropical Biological Resources, Ministry of Education, School of Life Science and Pharmacy, Hainan University, Haikou 570228, China | | | HU Wen-ting | Key Laboratory of Tropical Biological Resources, Ministry of Education, School of Life Science and Pharmacy, Hainan University, Haikou 570228, China | huwt_0@hainu.edu.cn |
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| Abstract: |
| 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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