The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, 266003, China.
Environ Sci Pollut Res Int. 2023 Sep;30(43):97128-97146. doi: 10.1007/s11356-023-29016-4. Epub 2023 Aug 16.
The long-distance migration of polycyclic aromatic hydrocarbons (PAHs) promotes their release into the marine environment, posing a serious threat to marine life. Studies have shown that PAHs have significant immunotoxicity effects on bivalves, but the exact mechanism of immunotoxicity remains unclear. This paper aims to investigate the effects of exposure to 0.4, 2, and 10 μg/L of benzo(a)pyrene (B[a]P) on the immunity of Chlamys farreri under environmental conditions, as well as the potential molecular mechanism. Multiple biomarkers, including phagocytosis rate, metabolites, neurotoxicity, oxidative stress, DNA damage, and apoptosis, were adopted to assess these effects. After exposure to 0.4, 2, and 10 μg/L B[a]P, obvious concentration-dependent immunotoxicity was observed, indicated by a decrease in the hemocyte index (total hemocyte count, phagocytosis rate, antibacterial and bacteriolytic activity). Analysis of the detoxification metabolic system in C. farreri revealed that B[a]P produced B[a]P-7,8-diol-9,10-epoxide (BPDE) through metabolism, which led to an increase in the expression of protein tyrosine kinase (PTK). In addition, the increased content of neurotransmitters (including acetylcholine, γ -aminobutyric acid, enkephalin, norepinephrine, dopamine, and serotonin) and related receptors implied that B[a]P might affect immunity through neuroendocrine system. The changes in signal pathway factors involved in immune regulation indicated that B[a]P interfered with Ca and cAMP signal transduction via the BPDE-PTK pathway or neuroendocrine pathway, resulting in immunosuppression. Additionally, B[a]P induced the increase in reactive oxygen species (ROS) content and DNA damage, as well as an upregulation of key genes in the mitochondrial pathway and death receptor pathway, leading to the increase of apoptosis rate. Taken together, this study comprehensively investigated the detoxification metabolic system, neuroendocrine system, and cell apoptosis to explore the toxic mechanism of bivalves under B[a]P stress.
多环芳烃（PAHs）的长距离迁移促进了它们向海洋环境中的释放，对海洋生物构成了严重威胁。研究表明，PAHs 对双壳类动物具有显著的免疫毒性作用，但确切的免疫毒性机制尚不清楚。本文旨在研究在环境条件下，暴露于 0.4、2 和 10μg/L 苯并[a]芘（B[a]P）对皱纹盘鲍（Chlamys farreri）免疫力的影响，以及潜在的分子机制。采用吞噬率、代谢物、神经毒性、氧化应激、DNA 损伤和细胞凋亡等多种生物标志物来评估这些影响。在暴露于 0.4、2 和 10μg/L B[a]P 后，明显观察到浓度依赖性免疫毒性，表现为血细胞指数（总血细胞计数、吞噬率、抗菌和溶菌活性）下降。分析皱纹盘鲍解毒代谢系统发现，B[a]P 通过代谢产生 B[a]P-7,8-二醇-9,10-环氧化物（BPDE），导致蛋白酪氨酸激酶（PTK）表达增加。此外，神经递质（包括乙酰胆碱、γ-氨基丁酸、脑啡肽、去甲肾上腺素、多巴胺和 5-羟色胺）及其相关受体含量的增加表明，B[a]P 可能通过神经内分泌系统影响免疫。参与免疫调节的信号通路因子的变化表明，B[a]P 通过 BPDE-PTK 通路或神经内分泌通路干扰 Ca 和 cAMP 信号转导，导致免疫抑制。此外，B[a]P 诱导活性氧（ROS）含量和 DNA 损伤增加，以及线粒体途径和死亡受体途径关键基因的上调，导致细胞凋亡率增加。综上所述，本研究综合研究了解毒代谢系统、神经内分泌系统和细胞凋亡，以探讨 B[a]P 胁迫下双壳类动物的毒性机制。
