The Infact Of Iron Copper On PrP-Gene-Transgenic Caenorhabditis Eegans Model

Nervous system diseases which caused by prion are fatal neurodegenerative diseases whose etiology islinked to the conversion of the cellular form of the prion protein （PrPc）. Recent researches show that Cu²⁺ isa key factor in the pathogenesis of Prion Protein （PrP）. PrPccan be transformed into an abnormalconformation of protease hydrolysis resistance, know as prion. Recent researches show that Cu²⁺is a keyfactor in the pathogenesis of prion protein, but whether the Cu²⁺is promotes or resistrains the conformationhas not yet been reached a final conclusion. Caenorhabditis elegans （C. elegans） as a model organism hasbeen used widely, and the transgenic c.elegans has been designed as research model of human relatedneurodegenerative diseases.In the present study, the basal slowing response （or food-sensing response） test, life span test and layingeggs statistical test of C. elegans were used to futher investigate the role of Cu²⁺in the pathologic processesinvolving the prion diseases. Research data show that when C.elegans was exposed to high concentration ofCu²⁺, W101（dat-1-PrPWt） which expressing PrP was damaged more severely than the wild type C.elegansN2. Similarly, the W102（dat-1-PrP102Mut）expressing mutations in the102site of PrP was damaged moreseverely than W101. According to the results, high concentration of Cu²⁺has a promoting effect on proindisease.This research is of some significance to give deep insight into the impact of cupric ion in the proindisease course, and is beneficial to clarify the nosogenesis of proin disease and more important to proindisease control.