Yu Keying, Yang Sirui, Song Hongxu, Sun Zhou, Wang Kaichao, Zhu Yuqi, Yang Chengkai, Hao Rongzhang, Cao Yuanyuan
Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, China.
Beijing Key Laboratory of Environment and Aging, Capital Medical University, Beijing 100069, China.
Biosensors (Basel). 2025 Apr 11;15(4):242. doi: 10.3390/bios15040242.
Brain aging is a complex process regulated by genetic, environmental, and metabolic factors, and increasing evidence suggests that environmental pollutants can significantly accelerate this process by interfering with oxidative stress, neuroinflammation, and mitochondrial function-related signaling pathways. Traditional studies have focused on the direct damage of pollutants on macromolecules (e.g., proteins, DNA), while the central role of senescence-associated small molecules (e.g., ROS, PGE2, lactate) in early regulatory mechanisms has been long neglected. In this study, we innovatively proposed a cascade framework of "small molecule metabolic imbalance-signaling pathway dysregulation-macromolecule collapse", which reveals that pollutants exacerbate the dynamics of brain aging through activation of NLRP3 inflammatory vesicles and inhibition of HIF-1α. Meanwhile, to address the technical bottleneck of small molecule spatiotemporal dynamics monitoring, this paper systematically reviews the cutting-edge detection tools such as electrochemical sensors, genetically encoded fluorescent probes and antioxidant quantum dots (AQDs). Among them, AQDs show unique advantages in real-time monitoring of ROS fluctuations and intervention of oxidative damage by virtue of their ultra-high specific surface area, controllable surface modification, and free radical scavenging ability. By integrating multimodal detection techniques and mechanism studies, this work provides a new perspective for analyzing pollutant-induced brain aging and lays a methodological foundation for early intervention strategies based on small molecule metabolic networks.
脑老化是一个由遗传、环境和代谢因素调节的复杂过程,越来越多的证据表明,环境污染物可通过干扰氧化应激、神经炎症和线粒体功能相关信号通路,显著加速这一过程。传统研究主要关注污染物对大分子(如蛋白质、DNA)的直接损伤,而衰老相关小分子(如活性氧、前列腺素E2、乳酸)在早期调节机制中的核心作用长期以来一直被忽视。在本研究中,我们创新性地提出了一个“小分子代谢失衡-信号通路失调-大分子崩溃”的级联框架,揭示了污染物通过激活NLRP3炎性小体和抑制缺氧诱导因子-1α,加剧脑老化的动态过程。同时,为解决小分子时空动态监测的技术瓶颈,本文系统综述了电化学传感器、基因编码荧光探针和抗氧化量子点(AQDs)等前沿检测工具。其中,AQDs凭借其超高的比表面积、可控的表面修饰和自由基清除能力,在实时监测活性氧波动和干预氧化损伤方面显示出独特优势。通过整合多模态检测技术和机制研究,本工作为分析污染物诱导的脑老化提供了新视角,并为基于小分子代谢网络的早期干预策略奠定了方法学基础。