Chen Ling, Zhu Mengyuan, Liu Yafeng, Yang Zhongchao, Li Huan, Mu Hongxin, Liu Su, Wu Bing
State Key Laboratory of Pollution Control and Resource Reuse, School of Environment, Nanjing University, Nanjing 210023, PR China.
Department of Environmental Science, School of Engineering, China Pharmaceutical University, Nanjing 211198, PR China.
Sci Total Environ. 2023 Mar 25;866:161261. doi: 10.1016/j.scitotenv.2022.161261. Epub 2022 Dec 29.
Perfluorobutanesulfonate (PFBS), an alternative to perfluorooctanesulfonate (PFOS), has raised many health concerns. However, PFBS toxicity in the mammalian gut remains unclear. C57BL/6 mice were exposed to 10 μg/L and 500 μg/L PFBS or 500 μg/L PFOS in their water supply for 28 days. PFBS toxicity in the ileum and colon was explored and compared to that of PFOS. Biochemical analysis showed that tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels increased in the ileum exposed to 10 μg/L PFBS, whereas no significant changes were observed in those levels in the colon. Catalase (CAT) activity, malondialdehyde (MDA), TNF-α, and IL-1β levels increased and glutathione (GSH) levels decreased in the ileum of the 500 μg/L-PFBS group, whereas only MDA levels increased in the colon of the 500 μg/L-PFBS group. The results showed that more severe damage occurred in the ileum than in the colon after PFBS exposure, and these align with the 500 μg/L-PFOS group exposure as well. Furthermore, metabolomic analysis revealed glutathione metabolism as a vital factor in inducing PFBS and PFOS toxicities in the ileum. Steroid hormone and amino acid metabolisms were other important factors involved in PFBS and PFOS toxicities, respectively. In the colon, GSH, pyrimidine, and glucose (especially galactose) metabolism was the main contributor to PFBS toxicity, and sulfur amino acid metabolism was the main pathway for PFOS toxicity. This study provides more evidence of the health hazards due to low-dose PFBS exposure in the mammalian gut.
全氟丁烷磺酸酯（PFBS）作为全氟辛烷磺酸酯（PFOS）的替代品，引发了诸多健康问题。然而，PFBS在哺乳动物肠道中的毒性仍不明确。将C57BL/6小鼠置于含有10μg/L和500μg/L PFBS或500μg/L PFOS的饮用水中28天。探究了PFBS在回肠和结肠中的毒性，并与PFOS进行比较。生化分析表明，暴露于10μg/L PFBS的回肠中肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）水平升高，而结肠中这些水平未观察到显著变化。500μg/L-PFBS组回肠中的过氧化氢酶（CAT）活性、丙二醛（MDA）、TNF-α和IL-1β水平升高，谷胱甘肽（GSH）水平降低，而500μg/L-PFBS组结肠中仅MDA水平升高。结果表明，PFBS暴露后回肠比结肠发生更严重的损伤，且这些结果与500μg/L-PFOS组暴露情况一致。此外，代谢组学分析揭示谷胱甘肽代谢是诱导PFBS和PFOS在回肠中产生毒性的关键因素。类固醇激素和氨基酸代谢分别是参与PFBS和PFOS毒性的其他重要因素。在结肠中，GSH、嘧啶和葡萄糖（尤其是半乳糖）代谢是PFBS毒性的主要促成因素，而含硫氨基酸代谢是PFOS毒性的主要途径。本研究为低剂量PFBS暴露对哺乳动物肠道造成健康危害提供了更多证据。
