Division of Spine Surgery, Department of Orthopaedics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Guangzhou Key Laboratory of Forensic Multi-Omics for Precision Identification, School of Forensic Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China.
Ecotoxicol Environ Saf. 2024 Feb;271:115866. doi: 10.1016/j.ecoenv.2023.115866. Epub 2024 Jan 9.
Triclosan (TCS), a broad-spectrum, lipophilic, and antibacterial agent, has been commonly used in cosmetics, medical devices, and household products. The toxicity of TCS has recently become a research hotspot. Emerging evidence has shown that TCS can easily migrate to humans and animals and cause adverse effects on various target organs. However, the effects of TCS exposure on nephrotoxicity and underlying mechanisms remain unknown. The aim of the present study was to explore TCS-induced nephrotoxicity. Therefore, we establish a mouse model based on adult male mice to explore the effects of 10-week TCS exposure (50 mg/kg) on kidney. After mice were sacrificed, their blood, feces, and renal tissues were harvested for further analysis. We found that TCS treatment dramatically caused kidney structural damage, and increased blood urea nitrogen (BUN) and creatinine (Cr) expression levels, which indicated renal dysfunction. In addition, TCS exposure increased the malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and total cholesterol (TCHO) expression levels, which indicated oxidative stress and lipid metabolism changes. The RNA sequencing (RNA-seq) of kidney tissue identified 221 differentially expressed genes (DEGs) enriched in 50 pathways, including drug metabolism-other enzymes, oxidative phosphorylation, glutathione metabolism, and inflammatory mediator regulation of TRP channels signaling pathways. The full-length 16S rRNA gene sequencing results showed that TCS exposure altered the community of gut microbiota, which was closely related to renal function damage. The above findings provide new insights into the mechanism of TCS-induced nephrotoxicity.
三氯生（TCS）是一种广谱、亲脂性、抗菌剂，广泛应用于化妆品、医疗器械和家用产品中。TCS 的毒性最近成为研究热点。新出现的证据表明，TCS 很容易迁移到人类和动物体内，并对各种靶器官造成不良影响。然而，TCS 暴露对肾毒性的影响及其潜在机制尚不清楚。本研究旨在探讨 TCS 诱导的肾毒性。因此，我们建立了一个基于成年雄性小鼠的小鼠模型，以探讨 10 周 TCS 暴露（50mg/kg）对肾脏的影响。处死小鼠后，采集其血液、粪便和肾脏组织进行进一步分析。我们发现 TCS 处理显著导致肾脏结构损伤，并增加了血尿素氮（BUN）和肌酐（Cr）的表达水平，表明肾功能障碍。此外，TCS 暴露增加了丙二醛（MDA）的表达水平，降低了超氧化物歧化酶（SOD）和总胆固醇（TCHO）的表达水平，表明氧化应激和脂质代谢变化。肾脏组织的 RNA 测序（RNA-seq）鉴定了 221 个差异表达基因（DEGs），这些基因富集在 50 条通路中，包括药物代谢-其他酶、氧化磷酸化、谷胱甘肽代谢和炎症介质调节 TRP 通道信号通路。全长 16S rRNA 基因测序结果表明，TCS 暴露改变了肠道微生物群落，这与肾功能损伤密切相关。上述发现为 TCS 诱导的肾毒性机制提供了新的见解。
