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典型文献
Expression of Thioredoxin System Protein Induced by Silica in Rat Lung Tissue
文献摘要:
Silicosis, a potentially fatal global occupational disease,?is?characterized?by?progressive?deterioration of pulmonary function and irreversible fibrosis resulting from crystalline silicon dioxide or silica inhalation. Extensive pieces of evidence[1-3] manifest that inhaled silica particles could directly or indirectly?cause?excess?generation?of?reactive?oxygen species (ROS), which plays a key role in the pathogenesis of silicosis. In order to maintain the cellular redox balance, the main function of thioredoxin (Trx)/thioredoxin reductase (TrxR) systems?is?to?scavenge?the?ROS.?TrxR,?as?a?reductase of Trx currently known only, has the function of antioxidation and scavenging free radicals[4]. In addition,?recent?in vitro?studies?demonstrate?that?Trx interacts directly with and inhibits the activity of apoptosis-regulating kinase-1 (ASK-1)[5]. The damaged?cell?of?lung?tissue?caused?by?ROS?may?be?an important link to ASK-1 triggered cell apoptosis. Zhu et?al.[1]?reported?that?silica?could?aggravate?oxidative stress and promote the development of silicosis in rat?lungs?after?silica?exposure?by?downregulating?the expression?of?TrxR?and?poor?Trx?activity.?The?specific mechanism of imbalance of reduction/oxidation status in silicosis is poorly understood. Our previous studies[6] demonstrated that oxidative stress in rats induced by silica leads to increased peroxiredoxins (Prxs)?protein?reactivity?to?resist?oxidative?stress,?and Trx as an electron donor is functionally associated with?Prxs.?Hence,?we?propose?a?hypothesis?that?silica exposure may lead to the disturbance of the function of the Trx/TrxR system, contributing to further?oxidative?damage.
文献关键词:
作者姓名:
GUAN Yi;LI Gai;LIU Nan;WANG Yong Heng;ZHOU Qiang;CHANG Mei Yu;ZHAO Lin Lin;YAO San Qiao
作者机构:
School of Public Health, North China University of Science and Technology, Tangshan 063210, Hebei, China;North China University of Science and Technology Affiliated Hospital,Tangshan 063000,Hebei,China;Xinxiang Medical University, Xinxiang 453003, Henan, China;School of Pharmacy,North China University of Science and Technology, Tangshan 063210, Hebei, China
引用格式:
[1]GUAN Yi;LI Gai;LIU Nan;WANG Yong Heng;ZHOU Qiang;CHANG Mei Yu;ZHAO Lin Lin;YAO San Qiao-.Expression of Thioredoxin System Protein Induced by Silica in Rat Lung Tissue)[J].生物医学与环境科学(英文版),2022(07):663-668
A类:
Silicosis,silicosis,peroxiredoxins,Prxs
B类:
Expression,Thioredoxin,System,Protein,Induced,by,Silica,Rat,Lung,Tissue,potentially,fatal,global,occupational,disease,characterized,progressive,deterioration,pulmonary,irreversible,fibrosis,resulting,from,crystalline,silicon,dioxide,silica,inhalation,Extensive,pieces,evidence,manifest,that,inhaled,particles,could,indirectly,excess,generation,reactive,oxygen,species,ROS,which,plays,key,role,pathogenesis,order,maintain,cellular,thioredoxin,reductase,TrxR,systems,scavenge,currently,known,only,has,antioxidation,scavenging,free,radicals,addition,recent,vitro,studies,interacts,inhibits,apoptosis,kinase,ASK,damaged,tissue,caused,may,be,important,link,triggered,Zhu,reported,aggravate,oxidative,stress,promote,development,lungs,after,exposure,downregulating,expression,specific,mechanism,imbalance,reduction,status,poorly,understood,Our,previous,demonstrated,rats,induced,leads,increased,protein,reactivity,resist,electron,donor,functionally,associated,Hence,we,propose,hypothesis,disturbance,contributing,further
AB值:
0.542375
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