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在废水中微塑料的微生物殖民加速了与氧化应激和胰岛素/IGF1信号通路相关的衰老过程
Haibo Chen1, Mengfan Chen2, Yulun Gu1
1Institute for Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai, 200444, PR China.
Environmental pollution (Barking, Essex : 1987)
|June 4, 2023
概括
微生物殖民改变了聚乙烯 (PS) 的特性,加速了C. elegans的衰老,比原始PS. 这种微塑料的衰老与氧化应激和胰岛素/IGF1信号通路有关.
科学领域:
- 环境毒理学环境毒理学
- 微塑料研究 微塑料研究
- 生物老龄化 生物老龄化
背景情况:
- 聚钢 (PS) 的毒性是已知的,但其对寿命和微生物殖民机制的影响尚不清楚.
- 微生物殖民改变了PS的物理化学特性,影响了细菌的粘附性.
研究的目的:
- 研究生物膜开发的PS (B-PS) 对Caenorhabditis elegans的寿命和衰老机制的影响.
- 为了比较B-PS与原始PS (V-PS) 的毒性.
主要方法:
- 在不同度下,C. elegans暴露于V-PS和B-PS.
- 对寿命,脂素积累,活性氧物种 (ROS) 生成和与氧化应激和胰岛素/IGF1信号传导 (IIS) 途径相关的基因表达的分析.
- 使用了野生型和突变的C. elegans菌株 (daf-16, daf-2, age-1, pdk-1, akt-1).
主要成果:
- 与V-PS (100μg/L) 相比,B-PS暴露 (10μg/L) 显著减少了C. elegans的平均寿命和增加了脂素积累.
- 暴露于B-PS引发了氧化应激,改变了gst-4::GFP表达,并影响了IIS通路基因,包括DAF-16转位.
- daf-2,age-1,pdk-1和akt-1中的突变部分挽救了寿命和脂素积累,而daf-16突变加剧了这些影响.
结论:
- 生物膜开发的PS通过氧化应激和IIS通路加速了C. elegans的衰老.
- DAF-2-AGE-1-PDK-1-AKT-1-DAF-16信号级联对调节C. elegans的寿命至关重要,以应对B-PS.
- 微塑料的微生物殖民带来了重大的环境风险.
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