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微塑料粒径依赖性毒性、氧化应激诱导以及对单巢轮虫(Brachionus koreanus)中 p-JNK 和 p-p38 的激活作用。

Microplastic Size-Dependent Toxicity, Oxidative Stress Induction, and p-JNK and p-p38 Activation in the Monogonont Rotifer (Brachionus koreanus).

机构信息

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

Department of Chemistry, College of Natural Sciences, Hanyang University , Seoul 04763, South Korea.

出版信息

Environ Sci Technol. 2016 Aug 16;50(16):8849-57. doi: 10.1021/acs.est.6b01441. Epub 2016 Aug 4.

DOI:10.1021/acs.est.6b01441
PMID:27438693
Abstract

In this study, we evaluated accumulation and adverse effects of ingestion of microplastics in the monogonont rotifer (Brachionus koreanus). The dependence of microplastic toxicity on particle size was investigated by measuring several in vivo end points and studying the ingestion and egestion using 0.05-, 0.5-, and 6-μm nonfunctionalized polystyrene microbeads. To identify the defense mechanisms activated in response to microplastic exposure, the activities of several antioxidant-related enzymes and the phosphorylation status of mitogen-activated protein kinases (MAPKs) were determined. Exposure to polystyrene microbeads of all sizes led to significant size-dependent effects, including reduced growth rate, reduced fecundity, decreased lifespan and longer reproduction time. Rotifers exposed to 6-μm fluorescently labeled microbeads exhibited almost no fluorescence after 24 h, while rotifers exposed to 0.05- and 0.5-μm fluorescently labeled microbeads displayed fluorescence until 48 h, suggesting that 6-μm microbeads are more effectively egested from B. koreanus than 0.05- or 0.5-μm microbeads. This observation provides a potential explanation for our findings that microbead toxicity was size-dependent and smaller microbeads were more toxic. In vitro tests revealed that antioxidant-related enzymes and MAPK signaling pathways were significantly activated in response to microplastic exposure in a size-dependent manner.

摘要

在这项研究中,我们评估了单殖轮虫(Brachionus koreanus)摄入微塑料的积累和不良影响。通过测量几个体内终点,并使用 0.05μm、0.5μm 和 6μm 非功能化聚苯乙烯微珠研究摄入和排泄,研究了微塑料毒性对粒径的依赖性。为了确定针对微塑料暴露激活的防御机制,测定了几种与抗氧化剂相关的酶的活性和丝裂原激活蛋白激酶(MAPKs)的磷酸化状态。暴露于所有尺寸的聚苯乙烯微珠均导致显著的尺寸依赖性效应,包括生长速率降低、繁殖力降低、寿命缩短和繁殖时间延长。暴露于 6μm 荧光标记微珠的轮虫在 24 小时后几乎没有荧光,而暴露于 0.05μm 和 0.5μm 荧光标记微珠的轮虫在 48 小时后仍显示荧光,表明 6μm 微珠比 0.05μm 或 0.5μm 微珠更有效地从 B. koreanus 中排出。这一观察结果为我们的发现提供了一个潜在的解释,即微珠毒性具有尺寸依赖性,较小的微珠毒性更大。体外试验表明,抗氧化剂相关酶和 MAPK 信号通路在微塑料暴露时以尺寸依赖性方式显著激活。

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