scholarly journals Stable expression of manganese superoxide dismutase (MnSOD) in insulinoma cells prevents IL-1beta- induced cytotoxicity and reduces nitric oxide production.

1998 ◽  
Vol 101 (9) ◽  
pp. 1811-1820 ◽  
Author(s):  
H E Hohmeier ◽  
A Thigpen ◽  
V V Tran ◽  
R Davis ◽  
C B Newgard
1995 ◽  
Vol 200 (2) ◽  
pp. 137-140 ◽  
Author(s):  
Eiji Kumura ◽  
Toshiki Yoshimine ◽  
Shigeki Kubo ◽  
Satonori Tanaka ◽  
Toru Hayakawa ◽  
...  

1996 ◽  
Vol 31 (4) ◽  
pp. 537-545 ◽  
Author(s):  
R. Tsunoda ◽  
K. Okumura ◽  
H. Ishizaka ◽  
T. Matsunaga ◽  
T. Tabuchi ◽  
...  

1995 ◽  
Vol 23 (2) ◽  
pp. 231S-231S
Author(s):  
Simon P. Fricker ◽  
Elizabeth Slade ◽  
Nigel A. Powell

2000 ◽  
Vol 192 (12) ◽  
pp. 1731-1744 ◽  
Author(s):  
Bernd van der Loo ◽  
Ralf Labugger ◽  
Jeremy N. Skepper ◽  
Markus Bachschmid ◽  
Juliane Kilo ◽  
...  

Vascular aging is mainly characterized by endothelial dysfunction. We found decreased free nitric oxide (NO) levels in aged rat aortas, in conjunction with a sevenfold higher expression and activity of endothelial NO synthase (eNOS). This is shown to be a consequence of age-associated enhanced superoxide (·O2−) production with concomitant quenching of NO by the formation of peroxynitrite leading to nitrotyrosilation of mitochondrial manganese superoxide dismutase (MnSOD), a molecular footprint of increased peroxynitrite levels, which also increased with age. Thus, vascular aging appears to be initiated by augmented ·O2− release, trapping of vasorelaxant NO, and subsequent peroxynitrite formation, followed by the nitration and inhibition of MnSOD. Increased eNOS expression and activity is a compensatory, but eventually futile, mechanism to counter regulate the loss of NO. The ultrastructural distribution of 3-nitrotyrosyl suggests that mitochondrial dysfunction plays a major role in the vascular aging process.


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