Wu Tianshu, Liu Kehan, Chen Siyuan, Ye Zongjian, Xia Jieyi, He Jing, Xing Pengcheng, Yang Jiafu, Qian Yijing, Chen Min
Key Laboratory of Environmental Medicine and Engineering, Ministry of Education, Nanjing 210009, China; School of Public Health, Southeast University, Nanjing 210009, China.
Key Laboratory of Environmental Medicine and Engineering, Ministry of Education, Nanjing 210009, China; School of Public Health, Southeast University, Nanjing 210009, China.
J Hazard Mater. 2025 Apr 5;487:137255. doi: 10.1016/j.jhazmat.2025.137255. Epub 2025 Jan 16.
Given the fact that carbon quantum dots (CQDs) have been commercially produced in quantities, it is inevitable to make their ways into environment and interact closely with the public. Even though CQDs in the environment have been reported to damage the central nervous system, the underlying mechanisms of neurotoxic effects of CQDs following respiratory exposure is still not clear. Intranasal instilled CQDs, mimicking respiratory exposure, induces neurobehavioral impairments associated with neuronal cell death of ferroptosis and disulfidptosis that is regulated by metabolic reprogramming of glutathione and cysteine pathways in the cortex and hippocampus where CQDs were hardly accumulated. Therefore, further exploration found that dysbiosis in the lung microbiome was found specifically manipulated by CQDs, which correlated with systemic and neuroinflammatory responses, implicating a lung-brain axis other than gut-brain axis as a critical pathway through which microbiota dysbiosis may impact neurological health after respiratory exposure to CQDs. This study pioneers the exploration of the neurological consequences of inhaled CQDs in the environment through the regulation of microbiome-lung-brain axis, which is key in understanding the mechanistic link between CQDs exposure and neurotoxicity. The findings could develop potential strategies for mitigating the neurological effects of CQDs even other types of nanoparticles.
鉴于碳量子点（CQDs）已实现商业化量产，它们进入环境并与公众密切接触在所难免。尽管已有报道称环境中的碳量子点会损害中枢神经系统，但碳量子点经呼吸道暴露后产生神经毒性作用的潜在机制仍不清楚。经鼻滴注碳量子点模拟呼吸道暴露，会诱发神经行为障碍，这与铁死亡和二硫化物诱导的神经元细胞死亡有关，而这种死亡是由皮质和海马体中谷胱甘肽和半胱氨酸途径的代谢重编程所调节的，而碳量子点在这些部位几乎不会积累。因此，进一步的探索发现，碳量子点会特异性地操纵肺部微生物群的生态失调，这与全身和神经炎症反应相关，这意味着除了肠-脑轴之外，肺-脑轴也是微生物群生态失调在呼吸道暴露于碳量子点后可能影响神经健康的关键途径。本研究率先通过微生物群-肺-脑轴的调节探索环境中吸入碳量子点的神经学后果，这对于理解碳量子点暴露与神经毒性之间的机制联系至关重要。这些发现可能会为减轻碳量子点甚至其他类型纳米颗粒的神经学影响制定潜在策略。
