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小球藻对三氯生和 6- 氯 - 二甲氧基 - 对 - 二氢 - 苯并噻喃的生物响应及腐殖酸的调控

Biological responses of alga Euglena gracilis to triclosan and galaxolide and the regulation of humic acid.

机构信息

Shenzhen Key Laboratory of Environmental Chemistry and Ecological Remediation, College of Chemistry and Environmental Engineering, Shenzhen University, Shenzhen, 518060, China.

Shenzhen Key Laboratory of Environmental Chemistry and Ecological Remediation, College of Chemistry and Environmental Engineering, Shenzhen University, Shenzhen, 518060, China.

出版信息

Chemosphere. 2022 Nov;307(Pt 1):135667. doi: 10.1016/j.chemosphere.2022.135667. Epub 2022 Jul 11.

DOI:10.1016/j.chemosphere.2022.135667
PMID:35835236
Abstract

Although the toxicity of triclosan (TCS) and galaxolide (HHCB) in freshwater has been reported, little study is shed light on their molecular toxicity mechanism and the regulation of humic acid (HA). In this work, freshwater algae E. gracilis was selected to explore these processes, and the molecular toxicity mechanism was analyzed by metabolomics. TCS was more toxic to E. gracilis than HHCB at 1 d exposure with the EC value of 0.76 mg L, but HHCB showed a higher toxicity as the exposure time prolonged. HA could alleviate the toxicity of TCS and HHCB, mainly due to the inhibition of TCS uptake and oxidative stress, respectively. The perturbations on a number of antioxidant defense-related metabolites in response to TCS or HHCB also indicated oxidative stress was a main toxicity mechanism. However, the exposure to HHCB resulted in more pronounced perturbations in the purine metabolism than TCS, implying that HHCB may pose a genetic toxicity on algae. It may explain the higher toxicity of HHCB to algae as the exposure time increased. These findings provide a comprehensive understanding on the ecological risks of TCS or HHCB in natural waters.

摘要

尽管三氯生(TCS)和 (HHCB)在淡水中的毒性已被报道,但关于它们的分子毒性机制以及腐殖酸(HA)的调节作用的研究甚少。在这项工作中,选择淡水藻类绿藻来探索这些过程,并通过代谢组学分析分子毒性机制。在 1 天的暴露时间内,TCS 对 E. gracilis 的毒性比 HHCB 更强,EC 值为 0.76mg/L,但随着暴露时间的延长,HHCB 的毒性更高。HA 可以减轻 TCS 和 HHCB 的毒性,主要是由于分别抑制了 TCS 的摄取和氧化应激。TCS 或 HHCB 对一些抗氧化防御相关代谢物的扰动也表明氧化应激是一种主要的毒性机制。然而,与 TCS 相比,HHCB 暴露导致嘌呤代谢的扰动更为明显,这表明 HHCB 可能对藻类具有遗传毒性。这可以解释 HHCB 随着暴露时间的增加对藻类的毒性更高的原因。这些发现为 TCS 或 HHCB 在天然水中的生态风险提供了全面的认识。

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引用本文的文献

1
Molecular Toxicity Mechanism Induced by the Antibacterial Agent Triclosan in Freshwater Based on the Transcriptome.基于转录组学的抗菌剂三氯生对淡水生物分子毒性机制研究
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