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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY · 2025 · IF 6.1

Bisphenol M exposure promotes adiposity in mice via disrupting hepatic metabolism and gut microbiota homeostasis

Xin Wang,Jie Zhao,Zehong Wu,Ling Wang,Wenjuan Zhang,Jie Zhang,Yong Liang

Bisphenol M (BPM), a structural analog of bisphenol A (BPA) commonly used in food packaging and consumer plastics, remains incompletely characterized in terms of its obesogenic potential and underlying molecular mechanisms, posing challenges for evidence-based risk assessment. To address this gap, we investigated the obesogenic effects and metabolic impacts of BPM exposure in male BALB/c mice through integrated liver untargeted metabolomics and gut microbiome analysis. Our results showed that BPM exposure significantly increased body fat percentage, enlarged the epididymal white adipose tissue volume, and induced hepatic steatosis. Untargeted metabolomics revealed that BPM disrupted hepatic metabolic pathways, such as riboflavin metabolism, glycerophospholipid metabolism and fatty acid degradation. Concurrently, BPM altered gut microbiota, increasing the Firmicutes/Bacteroidetes ratio and abundances of Staphylococcus and Jeotgalicoccus . Correlation networks linked these microbial shifts to hepatic lipid metabolites, specifically implicating linoleic acid metabolism as a potential mediator of gut-liver crosstalk in obesity development. These findings indicate that BPM promotes adiposity through liver-gut crosstalk, advancing the understanding of obesogenic risks associated with BPA alternatives.

CAS / MDL: 8001-30-7
研究领域: 毒理学 · 代谢研究 · 微生物组学
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CHEMOSPHERE · 2019 · IF 5.108

Enhanced degradation performance of bisphenol M using peroxymonosulfate activated by zero-valent iron in aqueous solution: Kinetic study and product identification

Jiayi Yao,Manqi Gao,Xiaofeng Guo,Fuxun Ai,Zunyao Wang

In the present work, we first examined the performance of zero-valent iron (Fe 0 ) activated peroxymonosulfate (PMS) for the removal of that bisphenol M (BPM). In 90 min, 95.9 ± 1.0% of BPM (initial concentration of 10 μM) could be removed in the optimal reaction conditions: [BPM] 0 :[PMS] 0  = 1:40 (molar ratio), [PMS] 0 :[Fe 0 ] 0  = 1:3 (molar ratio), pH = 8.0 (maintained by 0.1 M phosphate buffer solution), T = 35 °C. Common environmental ions like HCO 3 − , Cl − , NO 3 − accelerated BPM degradation while NH 4 + hindered it. In radical quenching tests, sulfate radicals (SO 4 − ) were found to play a dominant role in BPM degradation, while hydroxyl radicals ( OH) were also detected. By high-performance liquid chromatography–tandem mass spectrometry analysis, 13 products of BPM including small molecules, oligomers and hydroxylated derivatives were identified, and five possible degradation pathways were then proposed. The predicted acute toxicity of the reaction products was reduced after BPM was treated by Fe 0 /PMS. All these results prove that Fe 0 /PMS is an efficient, convenient, and environmentally friendly treatment method for the removal of BPM.

CAS / MDL: 299-11-6
研究领域: 环境科学 · 化学工程
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REPRODUCTIVE TOXICOLOGY · 2024 · IF 3.3

Bisphenol M inhibits mouse oocyte maturation in vitro by disrupting cytoskeleton architecture and cell cycle processes

Huilei Chen,Yang Liu,Yue Huang,Pin Zhang,Danli Du,Wenhua Yu,Caiyun Wu,Hongzhen Ruan,Ping Zhou,Zhiming Ding,Huifen Xiang

Bisphenol M (BPM), an alternative to bisphenol A (BPA), is commonly utilized in various industrial applications. However, BPM does not represent a safe substitute for BPA due to its detrimental effects on living beings. This research aimed to assess the influence of BPM exposure on the in vitro maturation of mouse oocytes. The findings revealed that BPM exposure had a notable impact on the germinal vesicle breakdown (GVBD) rate and polar body extrusion (PBE) rate throughout the meiotic progression of mouse oocytes, ultimately resulting in meiotic arrest. Investigations demonstrated that oocytes exposure to BPM led to continued activation of spindle assembly checkpoint. Further studies revealed that securin and cyclin B1 could not be degraded in BPM-exposed oocytes, and meiosis could not realize the transition from the MI to the AI stage. Mechanistically, BPM exposure resulted in abnormal spindle assembly and disrupted chromosome alignment of oocytes. Additionally, abnormal positioning of microtubule organizing center-associated proteins implied that MTOC may be dysfunctional. Furthermore, an elevation in the acetylation level of α-tubulin in oocytes was observed after BPM treatment, leading to decreased microtubule stability. In addition to its impact on microtubules, BPM exposure led to a reduction in the expression of the actin, signifying the disruption of actin assembly. Further research indicated a heightened incidence of DNA damage in oocytes following BPM exposure. Besides, BPM exposure induced alterations in histone modifications. The outcomes of this experiment demonstrate that BPM exposure impairs oocyte quality and inhibits meiotic maturation of mouse oocytes.

研究领域: 生殖生物学 · 细胞生物学 · 毒理学
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