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Nanoplastics promote arsenic-induced ROS accumulation, mitochondrial damage and disturbances in neurotransmitter metabolism of zebrafish (Danio rerio)
Summary
Researchers exposed zebrafish to nanoplastics combined with low concentrations of arsenic and found that nanoplastics significantly worsened arsenic's toxic effects on the brain. The mixture caused increased oxidative stress, mitochondrial damage, and disrupted neurotransmitter metabolism beyond what either pollutant caused alone. The study suggests that nanoplastics can act as carriers that amplify the neurotoxicity of other environmental contaminants in fish.
As a carrier, nanoplastics (NPs) can adsorb other toxic substances and thus modify their biological toxicity. Numerous studies have investigated the neurotoxic of high concentrations of arsenic (As, 2.83 mg/L-5 mg/L). However, it is still unknown whether the relatively low environmentally relevant concentrations of As (200 μg/L) can damage the structure and function of fish brains with the presence of NPs. In this study, zebrafish were exposed to polystyrene NPs, As and their mixture for 30 days respectively. Firstly, we found that the presence of NPs promoted the accumulation of As in zebrafish brains. Thereby the co-exposure of NPs and As further promoted the production of reactive oxygen species (ROS) in zebrafish brains compared with the single exposure of NPs or As, resulting in severe oxidative stress. Moreover, accumulated ROS directly damaged the mitochondrial membrane and mtDNA in zebrafish brains. Moreover, the mitochondrial damage was further aggravated due to inhibited mitochondrial fusion and activated mitochondrial division and mitophagy. Ultimately, the co-exposure led to mitochondrial damage in the zebrafish brain. Damaged mitochondria may not meet the high energy metabolic requirement for neuronal function. As a result, the normal function of nerve cells was adversely affected and eventually cell apoptosis may occur. Besides, the co-exposure caused more significant structural alterations in zebrafish brain tissue. Finally, the co-exposure of NPs and As caused abnormal biosynthesis and degradation of dopamine and acetylcholine. These resulted in decreased dopamine levels and increased acetylcholine levels in zebrafish brains. In conclusion, the presence of NPs promoted the accumulation of As, thereby inducing severe oxidative stress, which caused structural alterations and mitochondrial damage in the zebrafish brain, thus disordering neuromodulation, which may ultimately cause neurological dysfunction in zebrafish. This study will provide a risk assessment for evaluating the biotoxicity of NPs and As to fish and even other animals.
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