引用本文: | 郝其睿,张植元,王鹏,范泽,李晨辉,杨基先,王威.苯并芘对鲤鱼胆囊的毒性效应及响应机制[J].哈尔滨工业大学学报,2024,56(6):34.DOI:10.11918/202401092 |
| HAO Qirui,ZHANG Zhiyuan,WANG Peng,FAN Ze,LI Chenhui,YANG Jixian,WANG Wei.Toxic effects of benz[a]opyrene on gall bladder of common carp (Cyprinus carpio) and its response mechanism[J].Journal of Harbin Institute of Technology,2024,56(6):34.DOI:10.11918/202401092 |
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苯并芘对鲤鱼胆囊的毒性效应及响应机制 |
郝其睿1,2,张植元3,王鹏1,范泽4,李晨辉1,杨基先2,王威2
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(1.中国水产科学研究院黑龙江水产研究所 农业农村部渔业环境及水产品质量监督检验测试中心(哈尔滨),哈尔滨 150070; 2.哈尔滨工业大学 环境学院,哈尔滨 150090;3.四川水利职业技术学院 四川水利创新发展研究院,成都 611231; 4.黑龙江省水生动物病害与免疫重点试验室(中国水产科学研究院黑龙江水产研究所),哈尔滨 150070)
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摘要: |
为探讨苯并芘对鲤鱼胆囊的毒理机制,以鲤鱼(Cyprinus carpio)为试验材料,采用15 d慢性毒性试验(苯并芘质量浓度分别为0、0.025和0.25 mg/L),通过检测鲤鱼胆囊中苯并芘质量分数、抗氧化参数、转录应答及免疫基因表达。结果显示:胆囊组织中的苯并芘质量分数积累随着苯并芘胁迫质量浓度显著升高,侧面反映了胆囊在解毒和排毒过程中扮演着重要角色;B[a]P暴露后胆囊抗氧化酶活性(超氧化物歧化酶、过氧化氢酶及谷胱甘肽过氧化物酶)和丙二醛浓度均升高,表明机体可通过激活抗氧化酶系统以应对氧化应激;低质量浓度B[a]P暴露会引起鲤胆囊组织的免疫应答,激活Notch受体信号通路,进而引起细胞凋亡并消除自身组织中过多或异常的细胞;而高质量浓度B[a]P暴露会抑制RIG-I和Notch受体信号通路,引起胆囊免疫稳态失衡,细胞凋亡受到抑制,从而延长异常细胞的存活时间,并进一步激活免疫细胞,导致自身组织的损伤。本研究初步揭示了鲤胆囊细胞应对苯并芘暴露的可能自我保护机制,实现对水环境中多环芳烃污染的早期预警及生态风险评估提供理论基础。 |
关键词: 苯并芘 鲤鱼 胆囊 氧化应激 细胞凋亡 |
DOI:10.11918/202401092 |
分类号:S949 |
文献标识码:A |
基金项目:中国水产科学研究院中央级公益性科研院所基本科研业务费专项(2023TD60);中央级公益性科研院所基本科研业务费专项(HSY201904M) |
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Toxic effects of benz[a]opyrene on gall bladder of common carp (Cyprinus carpio) and its response mechanism |
HAO Qirui1,2,ZHANG Zhiyuan3,WANG Peng1,FAN Ze4,LI Chenhui1,YANG Jixian2,WANG Wei2
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(1.Supervision, Inspection and Testing Center for Fishery Environment and Aquatic Products(Harbin), Ministry of Agriculture and Rural Affairs,Heilongjiang River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Harbin 150070, China; 2.School of Environment, Harbin Institute of Technology, Harbin 150090, China; 3.Sichuan Water Conservancy Innovation and Development Research Institute,Sichuan Water Conservancy Vocational College, Chengdu 611231,China; 4.Key Laboratory of Aquatic Animal Diseases and Immune Technology of Heilongjiang Province (Heilongjiang River Fisheries Research Institute, Chinese Academy of Fishery Sciences), Harbin 150070,China)
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Abstract: |
To explore the toxicological mechanism of benz[a]opyrene (B[a]P) in gall bladder for aquatic animals, common carp (Cyprinus carpio) was used as the experimental material in this study. A 15-day chronic toxicity test was conducted with different concentrations of B[a]P (0,0.025 and 0.25 mg/L) exposure to examine the toxicological mechanisms of B[a]P on carp gall bladder by measuring the content of B[a]P, antioxidant parameters, transcriptional response and immune gene expressions in common carp gall bladder. Results show that the accumulation of B[a]P in gall bladder tissues increased significantly with the concentration of B[a]P stress, which indicates that gall bladder plays an important role in detoxification. The activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) and the concentration of malondialdehyde increased after B[a]P exposure, indicating that the gall bladder can respond to oxidative stress by activating the antioxidant oxidase system. In addition, exposure to low concentrations of B[a]P can induce immune responses in common carp gall bladder tissues, activating the Notch receptor signaling pathway, thereby causing apoptosis and eliminating excessive or abnormal cells in their own tissues. However, high-concentration exposure to B[a]P can inhibit the RIG-I and Notch receptor signaling pathways, causing an imbalance in gall bladder immune homeostasis. This inhibition of cell apoptosis prolongs the survival time of abnormal cells, and further activates immune cells, leading to self-tissue damage. This study provides preliminary insights into the potention self-protective mechanisms of common carp gall bladder cells in response to B[a]P exposure, laying the fundation for early warning and ecological risk assessment of polycyclic aromatic hydrocarbon pollution in water environment. |
Key words: benz[a]opyrene (B[a]P) common carp (Cyprinus carpio) gall bladder oxidative stress apoptosis |
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