光老化PET纳米塑料对海洋生物的神经毒性风险

Toxic and mechanism of light-aged PET nanoplastics on neuronal cells

  • 摘要: 纳米塑料广泛存在于海洋环境中,毒性风险会随其在环境中的老化加剧。然而,目前纳米塑料所诱发的海洋生物神经毒性效应及其形成机理尚未清楚。聚对苯二甲酸乙二醇酯(polyethylene terephthalate, PET)是海洋中最常见的纳米塑料之一。环境光老化过程可改变PET的理化性质,进而对海洋生物产生神经毒性效应。本研究以大鼠肾上腺嗜铬细胞瘤细胞(pheochromocytoma cells, PC 12)为模型,旨在探究光老化PET纳米塑料对海洋生物的神经毒性效应及潜在形成机理。结果表明,PET纳米塑料对PC 12的活力和多巴胺代谢能力均有抑制作用;当光老化PET纳米塑料的暴露浓度为20 μg/mL时,PC 12胞内的超氧化物歧化酶活性升高了6.73~8.24倍,谷胱甘肽过氧化物酶活性降低了4.55~5.26倍,丙二醛含量亦明显增加了2.03~5.12倍。本研究可为海洋环境中纳米塑料的生态风险评价提供新见解。

     

    Abstract: Nanoplastics are widely present in the marine environment and their toxicity risk increases with environmental ageing processes. However, the neurotoxic effects induced by nanoplastics in marine organisms and the mechanism of formation are not yet clear. Polyethylene terephthalate (PET) is one of the most common nanoplastics in the ocean. The environmental photoaging process can change its physicochemical properties, and then produce neurotoxic effects on marine organisms. In this study, rat adrenal pheochromocytoma cells (PC 12) were used as the model, aiming to investigate the neurotoxic effects of photoaging PET nanoplastics on marine organisms and the potential formation mechanism. The results showed that PET nanoplastics inhibited the viability and dopamine metabolism of PC 12, and the intracellular superoxide dismutase activity of PC 12 was increased by 6.73−8.24 times, glutathione peroxidase activity was decreased by 4.55−5.26 times, and the malondialdehyde content was increased by 2.03−5.12 times when the exposure concentration of light-aged PET nanoplastics was 20 μg/mL. This study may provide new insights into the ecological risk assessment of nanoplastics in the marine environment.

     

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