Thioredoxin nitration causes irreversible loss of its cardioprotective propertyEnglish Full Text

Ling Tao~(1),Yi-Min Zang~1,Hui-Rong Liu,~(2),Feng Gao~1,Xin-Liang Ma~1 Corresponding author(1.Department of Physiology,Fourth Military Medical University,Xi’an,Shaanxi,710032,China;2.Department of Physiology,Shanxi Medical University,Taiyuan,Xi′an,Shanxi 030001,China)

Abstract: AIM: The present study determined whether peroxynitrite may cause nitrative inactivation of thioredoxin（Trx）,a novel anti-oxidant and anti-apoptotic protein,thus facilitating myocardial apoptosis.METHODS and RESULTS: Exposure of recombinant Trx to 100 M of SIN-1,a peroxynitrite donor,resulted in significant Trx nitration as determined by Western blotting,indicating that cardiac Trx is sensitive to nitrative modification.To determine whether nitration of Trx may alter its cardioprotective effect,adult mice were subjected to 30 minutes myocardial ischemia and 3 hours（apoptosis） or 24 hours（infarct） of reperfusion and treated with vehicle,native or nitrated human Trx1（10 min before reperfusion）.Administration of native Trx1 significantly reduced post-ischemic myocardial apoptosis and decreased infarct size（P＜0.01）.However,in vitro incubation of thioredoxin with SIN-1（to nitrate Trx1） prior to its administration completely abolished thioredoxin’s cardioprotective effect.Moreover,when Trx1 was incubated with SIN-1 in the presence of hemoglobin（to scavenge NO） or SOD（to scavenge superoxide）,the cardioprotective effect of Trx1 was fully preserved.CONCLUSION: These results indicate that SIN-1 inactivates thioredoxin in a peroxynitrite-dependent fashion and suggest that peroxynitrite may exert its pro-apoptotic effect by nitrative inactivation of thioredoxin.

Keywords：

apoptosis; thioredoxin; protein nitration; ischemia/reperfusion;

DOI：
10.13191/j.chj.2005.04.5.taol.002
Series：
Subject：
Classification Code：
R541

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Thioredoxin nitration causes irreversible loss of its cardioprotective propertyEnglish Full Text

Ling Tao~(1),Yi-Min Zang~1,Hui-Rong Liu,~(2),Feng Gao~1,Xin-Liang Ma~1 Corresponding author(1.Department of Physiology,Fourth Military Medical University,Xi’an,Shaanxi,710032,China;2.Department of Physiology,Shanxi Medical University,Taiyuan,Xi′an,Shanxi 030001,China)

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