QS458. Reperfusion Injury Induces HEME Oxygenase-1 and NADPH Quinone Oxidoreductase-1 Enzymes in an in Vivo Model of Lung Ischemia Reperfusion Injury

2009 ◽  
Vol 151 (2) ◽  
pp. 303
Author(s):  
M. Latif ◽  
X. Li ◽  
S.J. Belsley ◽  
G.J. Todd ◽  
C.P. Connery ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
In Vivo Model ◽  
Heme Oxygenase 1 ◽  
Quinone Oxidoreductase

scholarly journals Inhibition of IL-1β secretion and mitochondria respiration by arsenite which acts on myocardial ischemia-reperfusion injury

2019 ◽  
Author(s):  
Min Li ◽  
Yingwu Mei ◽  
Jingeng Liu ◽  
Kaikai Fan ◽  
Xinyue Gu ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
In Vivo Model ◽  
Heme Oxygenase 1 ◽  
Biological Target ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

ABSTRACTArsenite (NaAsO2) is a potent toxin that significantly contributes to human pathogenesis. Chronic exposure to arsenite results in various diseases. The physiologically important biological target(s) of arsenite exposure is largely unknown. Here we found that transient sodium arsenite treatment (1) blocks nigericin or Rotenone induced IL-1β secretion; (2) inhibits mitochondrial respiration with complex I–linked substrate; (3) induces Heme oxygenase-1 (HO-1) in myocardial tissue. (4) attenuates the myocardial ischemia-reperfusion injury in an in vivo model of rats. The causal relationship among these activities needs further investigation.

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