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目的探讨多环芳烃(PAHS)与铅(Pb)联合暴露产生神经毒性的可能作用机制。方法用比较毒理基因组学数据库分析Pb和15种欧盟优先控制的PAHS共同影响的基因/蛋白及其中与神经系统疾病有关的基因/蛋白。通过文献分析这些基因/蛋白对神经系统损伤的可能机制。结果 Pb和15种PAHS可以影响的基因/蛋白有16个,其中有14个与神经系统疾病有关。这些基因/蛋白可以通过配体激活、细胞凋亡、氧化应激、炎症介质等途径造成神经系统损伤。结论 PAHS与Pb联合暴露可在分子水平上相互影响,造成神经系统损伤。
Objective To explore the possible mechanism of neurotoxicity induced by combined exposure of polycyclic aromatic hydrocarbons (PAHS) and lead (Pb). Methods Toxicogenomic genomic databases were used to analyze the genes / proteins that are commonly associated with Pb and 15 priority PAHS controlled by the European Union (EU) and the genes / proteins involved in these diseases. The possible mechanisms by which these genes / proteins damage the nervous system are analyzed by literature. Results There were 16 genes / proteins that Pb and 15 kinds of PAHS could affect, of which 14 were related to nervous system diseases. These genes / proteins can cause nervous system damage through ligand activation, apoptosis, oxidative stress and inflammatory mediators. Conclusion Combined exposure of PAHS and Pb can affect each other at the molecular level, resulting in nervous system damage.