College of Oceanography, Hohai University, Nanjing, Jiangsu 210098, PR China.
Laboratory for Earth Surface Processes, College of Urban and Environmental Sciences, Peking University, Beijing 100871, PR China.
Sci Total Environ. 2021 Aug 1;780:146587. doi: 10.1016/j.scitotenv.2021.146587. Epub 2021 Mar 19.
The adverse effects on model fish induced by methamphetamine (METH) have been revealed. However, the toxicity of METH on different kinds of non-model fish during the natural attenuation remained unclear. Hence, in this study, we for the first time established a static lab-scale aquatic ecosystem spiked with METH (initial levels at 25 μg/L) for 40 days to estimate its metabolism and toxicity in Chinese medaka, rosy bitterling, loach, and mosquito fish. The concentrations of METH in water and fish's brain were detected termly. The physiological functions, histopathology of brain, neurotransmitters contents, and expressions of associated genes of the four kinds of fish were determined at day 0, 20, and 40, respectively. The results indicated METH could be remarkably accumulated in fish brains with the distribution factor vs water (DFw) at 232.5-folds, and attenuated both in water and fish body during the exposure. METH caused physiological functions (i.e., swimming trajectories, locomotion distances, and feeding rates) disorders of the four kinds of fish, and stimulated surfacing behavior of loach. Tissue and macro/micromolecular biomarkers including histopathology, neurotransmitters (i.e., dopamine, serotonin, and norepinephrine), and mRNA, were similarly affected by METH. Mitogen-activated protein kinase (MAPKs) signaling pathway, P53-regulated apoptosis signaling pathway, N-methyl-d-aspartate-dopamine system, and mTOR signaling pathway of different kinds of fish were regulated by METH. Additionally, the impairments of the physiological and macromolecular indicators of fish could be alleviated as the natural attenuation of METH occurred. All the biomarkers, as well as the recovery effects during the exposure were integrated onto an adverse outcome pathway (AOP) framework. The key event was the micromolecular indicators (genes). The adverse outcomes at individual and population levels would result in the ecological consequences, implying the imperative to consider the natural attenuation process while assessing the environmental risk of METH.
已揭示出甲基苯丙胺（METH）对模式鱼类的不良影响。然而，在自然衰减过程中，METH 对不同种类的非模式鱼类的毒性仍不清楚。因此，在这项研究中，我们首次建立了一个静态实验室规模的水生生态系统，其中添加了 METH（初始浓度为 25μg/L），以评估其在中华斗鱼、玫瑰鲫、泥鳅和食蚊鱼中的代谢和毒性。定期检测水中和鱼类大脑中的 METH 浓度。分别在第 0、20 和 40 天测定了四种鱼类的生理功能、脑组织病理学、神经递质含量和相关基因的表达。结果表明，METH 可以在鱼脑中显著积累，其与水的分布因子（DFw）为 232.5 倍，并且在暴露期间，无论是在水中还是在鱼体内，METH 浓度都在衰减。METH 导致四种鱼类的生理功能（即游泳轨迹、运动距离和摄食率）紊乱，并刺激泥鳅浮出水面。组织和宏观/微观分子生物标志物，包括组织病理学、神经递质（即多巴胺、血清素和去甲肾上腺素）和 mRNA，也受到 METH 的类似影响。不同鱼类的丝裂原激活的蛋白激酶（MAPKs）信号通路、P53 调节的细胞凋亡信号通路、N-甲基-D-天冬氨酸-多巴胺系统和 mTOR 信号通路均受 METH 调节。此外，随着 METH 的自然衰减，鱼类的生理和宏观分子指标的损伤可以得到缓解。所有生物标志物以及暴露过程中的恢复效果都被整合到一个不良结局途径（AOP）框架中。关键事件是微观分子指标（基因）。个体和种群水平的不良后果将导致生态后果，这意味着在评估 METH 的环境风险时，必须考虑自然衰减过程。
