Key Laboratory of Integrated Regulation and Resource Development on Shallow Lakes, Ministry of Education, Hohai University, Nanjing, 210098, PR China; College of Environment, Hohai University, Nanjing, 210098, PR China.
Key Laboratory of Integrated Regulation and Resource Development on Shallow Lakes, Ministry of Education, Hohai University, Nanjing, 210098, PR China; College of Environment, Hohai University, Nanjing, 210098, PR China.
Chemosphere. 2024 Aug;362:142674. doi: 10.1016/j.chemosphere.2024.142674. Epub 2024 Jun 20.
Triclocarban (TCC), an emerging contaminant in water environments, its effects on freshwater biofilms remain insufficiently understood. This study investigates the effects of TCC exposure (at concentrations of 10 μg L and 10 mg L) on mature freshwater biofilms. TCC was found to inhibit biofilm activity as evidenced by changes in surface morphology and the ratio of live/dead cells. Moreover, both concentrations of TCC were observed to modify the structure of the biofilm community. Metabolomics analysis revealed an overlap in the toxicity mechanisms and detoxification strategies triggered by various concentrations of TCC in biofilms. However, the higher toxicity induced by 10 mg L TCC resulted from the downregulation of proline betaine, disrupting the homeostasis of cellular osmotic pressure regulation in biofilms. Notably, lipid and lipid-like molecules showed high sensitivity to different concentrations of TCC, indicating their potential as biomarkers for TCC exposure. Annotation of the differential metabolites by KEGG revealed that alterations in amino acid and carbon metabolism constituted the primary response mechanisms of biofilms to TCC. Moreover, the biofilm demonstrated enhanced nucleic acid metabolism, which bolstered resistance against TCC stress and heightened tolerance. Furthermore, elevated TCC concentrations prompted more robust detoxification processes for self-defense. Overall, short-term exposure to TCC induced acute toxicity in biofilms, yet they managed to regulate their community structure and metabolic levels to uphold oxidative homeostasis and activity. This research contributes to a deeper comprehension of TCC risk assessment and policy control in aquatic environments.
三氯卡班（TCC）是一种新兴的水环境污染物，其对淡水生物膜的影响尚未得到充分认识。本研究调查了 TCC 暴露（浓度为 10μg/L 和 10mg/L）对成熟淡水生物膜的影响。研究发现 TCC 抑制了生物膜活性，表现为表面形态和活/死细胞比例的变化。此外，两种浓度的 TCC 都观察到改变了生物膜群落的结构。代谢组学分析表明，不同浓度的 TCC 在生物膜中触发的毒性机制和解毒策略存在重叠。然而，10mg/L TCC 引起的更高毒性是由于脯氨酸甜菜碱的下调，破坏了生物膜中细胞渗透压调节的内稳态。值得注意的是，脂质和类脂分子对不同浓度的 TCC 表现出高敏感性，表明它们可能成为 TCC 暴露的生物标志物。通过 KEGG 对差异代谢物进行注释表明，氨基酸和碳代谢的改变构成了生物膜对 TCC 的主要响应机制。此外，生物膜表现出增强的核酸代谢，这增强了对 TCC 应激的抵抗力和耐受性。此外，较高的 TCC 浓度促使更强的解毒过程进行自我防御。总的来说，短期暴露于 TCC 会导致生物膜产生急性毒性，但它们能够调节其群落结构和代谢水平，以维持氧化平衡和活性。这项研究有助于更深入地了解 TCC 在水生环境中的风险评估和政策控制。
