The fine particulate matter (PM2.5) in air pollution is a major public health concern and now known to contribute to severe diseases, therefore, a comprehensive understanding of PM2.5-induced adverse effects in living organisms is needed urgently. This study was aimed to evaluate the toxicity of PM2.5 on multi-organ systems in a zebrafish (Danio rerio) model. The embryonic toxicity induced by PM2.5 was demonstrated by an increase in mortality and inhibition of hatching rate, in a dose- and time-dependent manner. PM2.5 caused the pericardial edema, as well as reducing heart rate and cardiac output. The area of sub-intestinal vessels (SIVs) was significant reduced in Tg(fli-1:EGFP) transgenic zebrafish lines. Morphological defects and yolk sac retention were associated with hepatocyte injury. In addition, PM2.5 disrupted the axonal integrity, altering of axon length and pattern in Tg(NBT:EGFP) transgenic lines. Genes involved in cardiac function (spaw, supt6h, cmlc1), angiogenesis (vegfr2a, vegfr2b), and neural function (gabrd, chrna3, npy8br) were markedly down-regulated; while genes linked to hepatic metabolism (cyp1a, cyp1b1, cyp1c1) were significantly up-regulated by PM2.5. In summary, our data showed that PM2.5 induced the cardiovascular toxicity, hepatotoxicity and neurotoxicity in zebrafish, suggested that PM2.5 could cause multi-organ toxicity in aquatic organism.
Keywords: Air pollution; Cardiovascular toxicity; Hepatotoxicity; Neurotoxicity; PM(2.5); Zebrafish.
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