摘要
氟中毒可造成机体的骨相和非骨相组织损害，其发生机制不清。大量研究证明，氟能引起机体各系统或脏器的蛋白合成下降、细胞凋亡增加，从而造成机体组织的广泛损伤，并且损伤机制可能与内质网应激有关。蛋白激酶受体样内质网激酶／磷酸化真核翻译起始因子2α（PERK／p-eIF2a）通路为内质网应激最先活化的通路，可能在氟中毒的发生机制中有重要作用。因此，作者将对PERK／p-eIF2a路在氟致机体损伤中的作用进行综述，以期为氟中毒发病机制的阐明和防治提供新思路。
Fluoride can cause phrenology and non-phrenology damage, but the mechanisms were unclear. It is reported that fluoride can decrease protein synthesis and induce cell apoptosis, leading to extensive systemic damage. Many studies have found that the mechanism is closely associated with endoplasmic retieulum stress. Protein kinase receptor-like ER kinase/Eukaryotic translation initiation factor 2α （PERK/eIF2α） signaling pathway is the first activation pathway when endoplasmic reticulum stress occurs which may play an important role in the pathogenesis of fluorosis. This present paper is focused on the role of PERK/eIF2α signaling pathway-related factors in the systemic and organism damages resulted from fluorosis, which may provide new ideas in mechanism and prevention of fluorosis.
出处
《中华地方病学杂志》
CAS
CSCD
北大核心
2016年第9期698-702,共5页
Chinese Journal of Endemiology
基金
国家自然科学基金（81502762）
教育部留学回国人员科研启动基金（教外司留2015331）
黑龙江省卫生厅科研课题（2013131）
