微塑料和DEHP的多物种联合毒性:陆生、水生动物与植物
Multi-species Combined Toxicity of Microplastics and DEHP: Terrestrial and Aquatic Animals and Plants
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摘要: 微塑料(MPs)与邻苯二甲酸二(2-乙基己基)酯(DEHP)作为环境中广泛存在的污染物,其单一及复合毒性效应对陆生动物、水生动物和植物的生态健康构成了严重威胁。笔者系统综述了MPs与DEHP对不同生物类群的毒性作用及其机制,揭示了复合污染的协同或拮抗效应,为生态风险评估提供了重要理论依据。在陆生动物中,MPs单独暴露可诱发肝脏炎症、氧化应激及肠道菌群失衡,并导致神经系统功能异常。MPs与DEHP联合暴露时,毒性效应显著增强,表现为多器官协同损伤:通过活性氧(ROS)介导的线粒体凋亡和坏死性凋亡途径导致肝细胞死亡;肾脏中氧化应激与炎症反应加剧;肠道通透性增加引发全身性炎症;生殖系统则因激素失衡和血-睾屏障破坏而功能受损。对水生动物的研究表明,MPs单独暴露可导致鳃组织损伤、生殖功能障碍及神经递质紊乱。DEHP与MPs联合暴露时,双壳贝类的滤食率显著下降,抗氧化系统崩溃,代谢途径(如能量代谢和脂质代谢)严重紊乱。此外,复合污染还引发斑马鱼幼体心脏发育畸形和大口黑鲈肠道绒毛结构破坏,凸显其对水生生物发育与生存的长期危害。植物实验显示,MPs抑制种子萌发(如番茄)、降低叶绿素含量(如烟草)并诱导氧化应激(如豌豆)。MPs与DEHP的复合效应因物种而异:在黄瓜中表现为抗氧化酶活性的拮抗作用,而在玉米中则协同抑制生长和光合作用,表明污染物的相互作用具有复杂性。综上所述,微塑料和DEHP联合暴露对陆生、水生动物以及植物均产生了比单一暴露更强的毒性效应,但是毒性靶点不同,导致了毒性效应的差异。当前研究在毒性机制深度解析、生态系统层面评估及环境因素交互作用等方面仍存在不足,未来需结合多组学技术和生态模拟实验,为复合污染的生态风险防控提供更全面的理论支撑。
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关键词:
- 微塑料 /
- 邻苯二甲酸二(2-乙基己基)酯 /
- 复合毒性 /
- 生态毒理
Abstract: Microplastics (MPs) and di(2-ethylhexyl) phthalate (DEHP) are ubiquitous environmental pollutants. Their individual and combined toxicological effects pose significant threats to the ecological health of terrestrial animals, aquatic organisms, and plants. This study systematically reviews the toxicological impacts of MPs and DEHP on various biological groups, elucidating their mechanisms and revealing both synergistic and antagonistic effects of co-exposure. These findings provide a critical theoretical foundation for ecological risk assessment. Among terrestrial animals, exposure to MPs alone can induce liver inflammation, oxidative stress, and intestinal flora imbalance, and lead to abnormal neurological function. When MPs and DEHP are exposed jointly, the toxic effects are significantly enhanced, manifesting as multi-organ coordinated damage: liver cell death is caused through the ROS-mediated mitochondrial apoptosis and necroptosis pathways. Oxidative stress and inflammatory responses are intensified in the kidneys; intestinal permeability increases, triggering systemic inflammation; and the reproductive system is impaired due to hormonal imbalance and disruption of the blood-testis barrier. Studies on aquatic animals have shown that exposure to MPs alone can lead to gill tissue damage, reproductive dysfunction, and neurotransmitter disorders. When DEHP and MPs are co-exposed, the filtration rate of bivalves significantly decreases, the antioxidant system collapses, and metabolic pathways (such as energy metabolism and lipid metabolism) are severely disrupted. Moreover, combined pollution causes cardiac developmental malformations in zebrafish larvae and destruction of intestinal villi structure in largemouth bass, highlighting the long-term harm to the development and survival of aquatic organisms. Plant experiments have demonstrated that MPs inhibit seed germination (such as in tomatoes), reduce chlorophyll content (such as in tobacco), and induce oxidative stress (such as in peas). The combined effects of MPs and DEHP vary by species: in cucumbers, it shows an antagonistic effect on antioxidant enzyme activity, while in corn, it synergistically inhibits growth and photosynthesis, indicating the complexity of the interaction between pollutants. To sum up, the combined exposure of MPs and DEHP has exerted stronger toxic effects on terrestrial, aquatic animals and plants than single exposure. However, the distinct toxic targets have resulted in the variations of toxic effects. In the future, it is necessary to combine multi-omics technology and ecological simulation experiments to provide more comprehensive theoretical support for the ecological risk prevention and control of combined pollution.-
Key words:
- microplastics /
- di-(2-ethylhexyl) phthalate /
- combined toxicity /
- ecotoxicology
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