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纳米塑料摄入通过多药耐药(MXR)破坏增强了单殖轮虫 Brachionus koreanus 中持久性有机污染物(POPs)的毒性。

Nanoplastic Ingestion Enhances Toxicity of Persistent Organic Pollutants (POPs) in the Monogonont Rotifer Brachionus koreanus via Multixenobiotic Resistance (MXR) Disruption.

机构信息

Department of Biological Science, College of Science , Sungkyunkwan University , Suwon 16419 , South Korea.

Pathology Division , National Institute of Fisheries Science , Busan 46083 , South Korea.

出版信息

Environ Sci Technol. 2018 Oct 2;52(19):11411-11418. doi: 10.1021/acs.est.8b03211. Epub 2018 Sep 14.

DOI:10.1021/acs.est.8b03211
PMID:30192528
Abstract

Among the various materials found inside microplastic pollution, nanosized microplastics are of particular concern due to difficulties in quantification and detection; moreover, they are predicted to be abundant in aquatic environments with stronger toxicity than microsized microplastics. Here, we demonstrated a stronger accumulation of nanosized microbeads in the marine rotifer Brachionus koreanus compared to microsized ones, which was associated with oxidative stress-induced damages on lipid membranes. In addition, multixenobiotic resistance conferred by P-glycoproteins and multidrug resistance proteins, as a first line of membrane defense, was inhibited by nanoplastic pre-exposure, leading to enhanced toxicity of 2,2',4,4'-tetrabromodiphenyl ether and triclosan in B. koreanus. Our study provides a molecular mechanistic insight into the toxicity of nanosized microplastics toward aquatic invertebrates and further implies the significance of synergetic effects of microplastics with other environmental persistent organic pollutants.

摘要

在微塑料污染中发现的各种物质中,由于难以量化和检测,纳米级微塑料尤其令人关注;此外,预计它们在水生环境中会很丰富,毒性比微米级微塑料更强。在这里,我们证明了与微米级微珠相比,纳米级微珠在海洋轮虫 Brachionus koreanus 中的积累更强,这与氧化应激诱导的脂质膜损伤有关。此外,由 P-糖蛋白和多药耐药蛋白赋予的多药耐药性作为第一道膜防御被纳米塑料预先暴露所抑制,导致 2,2',4,4'-四溴二苯醚和三氯生对 B. koreanus 的毒性增强。我们的研究提供了对纳米级微塑料对水生无脊椎动物毒性的分子机制见解,并进一步表明微塑料与其他环境持久性有机污染物协同效应的重要性。

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