Interactive effects of nitrite and bifenthrin on bioaccumulation, oxidative stress and immune responses of Haliotis discus hannai
文献类型：期刊论文
| 作者 | Chen, Hao5; Wu, Guiqing4; Jiao, Chunli1; Chen, Lizhu2; Sun, Chunxiao2; Zhang, Xinze2; Wei, Xiao2; Wu, Xueping4; Yang, Dinglong3; Zhao, Jianmin3 |
| 刊名 | AQUATIC TOXICOLOGY
 |
| 出版日期 | 2025-10-01 |
| 卷号 | 287页码:10 |
| 关键词 | Haliotis discus hannai Nitrite Bifenthrin Transcriptomics Immune function |
| ISSN号 | 0166-445X |
| DOI | 10.1016/j.aquatox.2025.107512 |
| 通讯作者 | Wu, Xueping(wxuep2020@163.com) ; Yang, Dinglong(dlyang@yic.ac.cn) |
| 英文摘要 | Nitrite (NO2-) and bifenthrin (BF), common environmental pollutant, have been proven to perform toxic effects on marine organisms. To have a better understanding of their effects on marine organism, Haliotis discus hannai was exposed to 0.1 mg/L NO2- and/or 10 mu g/L BF for 28 days. The results showed that the gills in direct contact with the water environment exhibited the highest levels of BF bioaccumulation (89.37-142.36 mu g/kg), especially after NO2- exposure (P < 0.05). Transcriptome analysis of gills showed that significant enrichments were observed in metabolic, signaling and immune pathways after exposure, such as cGMP-PKG signaling pathway. Additionally, superoxide dismutase (SOD) activity was decreased in gills after exposure to NO2- and/or BF, parallel with the increase in catalase (CAT) activity, malondialdehyde (MDA) content, and total antioxidant capacity (AOC). Regarding genes related to immune, the expression of Defensin was significantly decreased while the expressions of B-cell lymphoma-2 (Bcl-2), Tumor Necrosis Factor-alpha (TNF-alpha) and Caspase3 were increased. These results suggested that NO2- and BF exposure disrupted metabolic processes, impaired immune function, and dysregulated antioxidant defenses in the gills of abalone. Particularly, significant alterations were observed under the combined stress of NO2- and BF. In hemocytes, the ROS production could be induced by NO2- and/or BF stress, and the number of hemocytes and phagocytosis decreased significantly, especially in NO2- and BF groups. Integrated biomarker response (IBR) analysis proved that NO2- and/or BF exposure detrimentally affected the overall fitness of abalone, and combined NO2- and BF stress was the most stressful condition. This study emphasizes the impact of NO2- and/or BF on the abalone to better elucidate the risk of environmental pollution on abalone. |
| WOS关键词 | AMMONIA EXPOSURE ; TOXICITY ; WATER |
| WOS研究方向 | Marine & Freshwater Biology ; Toxicology |
| 语种 | 英语 |
| WOS记录号 | WOS:001541021800001 |
| 资助机构 | National Natural Science Foundation of China ; Natural Science Foundation of Shandong Province |
| 源URL | [http://ir.yic.ac.cn/handle/133337/41233]  |
| 专题 | 海岸带生物学与生物资源利用重点实验室 |
| 通讯作者 | Wu, Xueping; Yang, Dinglong |
| 作者单位 | 1.Yantai Ctr Food & Drug Control, Yantai 264003, Peoples R China 2.Shandong Marine Resources & Environm Res Inst, Shandong Key Lab Marine Ecol Restorat, Yantai 264006, Peoples R China 3.Chinese Acad Sci, Yantai Inst Coastal Zone Res, Res & Dev Ctr Efficient Utilizat Coastal Bioresour, Yantai 264003, Peoples R China 4.GuangXi MinZu Univ, Sch Marine Sci & Biotechnol, Nanning 530006, Guangxi, Peoples R China 5.Ludong Univ, Sch Resources & Environm Engn, Yantai 264025, Peoples R China |
| 推荐引用方式 GB/T 7714 | Chen, Hao,Wu, Guiqing,Jiao, Chunli,et al. Interactive effects of nitrite and bifenthrin on bioaccumulation, oxidative stress and immune responses of Haliotis discus hannai[J]. AQUATIC TOXICOLOGY,2025,287:10. |
| APA | Chen, Hao.,Wu, Guiqing.,Jiao, Chunli.,Chen, Lizhu.,Sun, Chunxiao.,...&Zhao, Jianmin.(2025).Interactive effects of nitrite and bifenthrin on bioaccumulation, oxidative stress and immune responses of Haliotis discus hannai.AQUATIC TOXICOLOGY,287,10. |
| MLA | Chen, Hao,et al."Interactive effects of nitrite and bifenthrin on bioaccumulation, oxidative stress and immune responses of Haliotis discus hannai".AQUATIC TOXICOLOGY 287(2025):10. |
入库方式： OAI收割
来源：烟台海岸带研究所
浏览0
下载0
收藏0
其他版本
除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。