Simplification on a kinetic model network related to hydrogen peroxide metabolism in human erythrocytes

Author(s):  
Patricia P. Grof ◽  
Yeung Yam
2014 ◽  
Vol 74 ◽  
pp. 35-49 ◽  
Author(s):  
Rui Benfeitas ◽  
Gianluca Selvaggio ◽  
Fernando Antunes ◽  
Pedro M.B.M. Coelho ◽  
Armindo Salvador

2014 ◽  
Vol 16 (27) ◽  
pp. 13595-13600 ◽  
Author(s):  
T. Poux ◽  
A. Bonnefont ◽  
A. Ryabova ◽  
G. Kéranguéven ◽  
G. A. Tsirlina ◽  
...  

A kinetic model sheds light on the mechanism of the hydrogen peroxide reactions on Mn- and Co-perovskite oxides.


1989 ◽  
Vol 256 (2) ◽  
pp. H584-H588 ◽  
Author(s):  
J. M. Brown ◽  
M. A. Grosso ◽  
L. S. Terada ◽  
C. J. Beehler ◽  
K. M. Toth ◽  
...  

Reperfusion with untreated, carbon monoxide-treated, or glutaraldehyde-fixed human erythrocytes (RBC) increased ventricular function and decreased myocardial hydrogen peroxide (H2O2) levels [assessed by H2O2-dependent aminotriazole (AMT) inactivation of myocardial catalase activities] of ischemic, isolated rat hearts. In contrast, reperfusion with RBC that lacked catalase (AMT treated) and/or glutathione (N-ethylmaleimide treated) did not increase ventricular function or decrease myocardial H2O2 levels as much as reperfusion with untreated RBC. By comparison, reperfusion with superoxide dismutase-depleted (diethyldithiocarbamate-treated) or anion channel-inhibited (diisothiocyanodisulfonic acid stilbene-treated) RBC increased ventricular function and decreased myocardial H2O2 levels the same as untreated RBC. The results suggest that catalase and/or glutathione in intact RBC can decrease endogenously generated H2O2 and related reperfusion injury in ischemic, isolated perfused hearts.


1974 ◽  
Vol 45 (1) ◽  
pp. 39-52 ◽  
Author(s):  
Gerhard Gerber ◽  
Heidemarie Preissler ◽  
Reinhart Heinrich ◽  
Samuel M. Rapoport

2012 ◽  
Vol 187 ◽  
pp. 36-44 ◽  
Author(s):  
M.D. Murcia ◽  
M. Gómez ◽  
E. Gómez ◽  
J.L. Gómez ◽  
A.M. Hidalgo ◽  
...  

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