title: The ROS-mediated pathway coupled with the MAPK-p38 signalling pathway and antioxidant system plays roles in the responses of Mytilus edulis haemocytes induced by BDE-47.
abstract: Our previous study found that BDE-47 could change the immune function of haemocytes in Mytilus edulis, and reactive oxygen species (ROS) might be involved in the process of physiological alteration. Here, we aimed to better understand this relationship. To accomplish this, we analysed changes in different ROS as well as various antioxidant system components. Additionally, the expression of MAPK-p38, a signalling protein regulated by ROS that helps to regulate numerous cellular processes, was also analysed. BDE-47 was given at low, medium, and high amounts. The results showed that (1) BDE-47 significantly affected ROS component levels in haemocytes. O2-content was increased under all conditions. H2O2content was also increased under all conditions, except in the middle concentration group. In contrast, OH content was increased in the low and middle concentration groups and decreased in the high concentration group. (2) Estimations of the antioxidant systems revealed concentration-dependent changes. Catalase activity was increased throughout the experiment, while superoxide dismutase (SOD) exhibited a decreasing trend in the tested groups with an increase of exposure time. On day 21, only the high concentration group showed a slight increase in SOD activity compared to the control. Furthermore, glutathione peroxidase and glutathione reductase activity increased in the low and middle concentration groups but decreased in the high concentration group. The GSH/GSSG ratio increased for all treatments over time, indicating that changes in redox status occurred. (3) MAPK-p38 was activated following BDE-47 exposure. Based on our previous study, we speculate that BDE-47 exposure induces ROS production and affects the ROS-mediated pathway, which may explain the resultant functional damage observed in haemocytes. Furthermore, BDE-47 also affected the antioxidant system and altered redox status, although these changes did not ameliorate the damage caused by ROS.
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: 1169753893@qq.com.
authors.forename: Yongshun
authors.initials: Y
authors.lastname: Jiang
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: tangxx@ouc.edu.cn.
authors.forename: Xuexi
authors.initials: X
authors.lastname: Tang
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: zhoubin@ouc.edu.cn.
authors.forename: Bin
authors.initials: B
authors.lastname: Zhou
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: suntianli89@126.com.
authors.forename: Tianli
authors.initials: T
authors.lastname: Sun
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: melissa821@foxmail.com.
authors.forename: Hongmei
authors.initials: H
authors.lastname: Chen
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: xyzhao331@gmail.com.
authors.forename: Xinyu
authors.initials: X
authors.lastname: Zhao
authors.affiliation: Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China. Electronic address: wangyou@ouc.edu.cn.
authors.forename: You
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D055768:Halogenated Diphenyl Ethers / Q000633:toxicity*; D006434:Hemocytes / Q000187:drug effects* / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D049880:Mytilus edulis / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity*
chemical_list: D000975:Antioxidants; D055768:Halogenated Diphenyl Ethers; D017382:Reactive Oxygen Species; D014874:Water Pollutants, Chemical; C511295:2,2',4,4'-tetrabromodiphenyl ether; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione
keywords: 2,2’,4,4’-Tetrabromodiphenyl ether (BDE-47); Antioxidant enzymes; Haemocytes; MAPK-p38 pathway; Reactive oxygen species (ROS) content