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-eIF2α)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-eIF2α通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.

abstractsFluoride 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 reticulum 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/elF2α signaling pathway-related factors in the systemic and organism damages resulted from fluorosis,which may provide new ideas in mechanism and prevention of fluorosis.