Assessment on the adverse effects on different kinds of fish induced by methamphetamine during the natural attenuation process based on adverse outcome pathway.

Abstract

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 25μg/L) for 40days 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.