Astrocytes overexpressing Cu,Zn superoxide dismutase have increased resistance to oxidative injury

Astrocytes overexpressing Cu,Zn superoxide dismutase have increased resistance to oxidative injury Overexpression of Cu,Zn SOD (SOD1) can increase survival of neurons under some pathological conditions. Prior studies have shown, however, that SOD1 overexpression can reduce neuronal survival during exposure to superoxide generators by a mechanism involving excess H2O2 accumulation. Since astrocytes exhibit greater H2O2 catabolism capacity than do neurons, the present study examined the effects of SOD1 overexpression on astrocyte survival under these conditions. Cultures were prepared from transgenic mice that overexpress human SOD1 and from nontransgenic littermate controls. Exposure to xanthine oxidase/hypoxanthine (XO/HPX) or menadione caused dose‐dependent astrocyte death. In contrast to prior observations with neurons, astrocytes that overexpress SOD1 showed increased resistance to superoxide toxicity. Surprisingly, increased survival in SOD1 overexpressing cultures remained evident even when H2O2 catabolism was inhibited by preincubation with aminotriazole (to block catalase) and buthionine sulfoximine (to deplete glutathione). These findings suggest differences in superoxide metabolism between neurons and astrocytes, and that the greater resistance of astrocytes to oxidative stress is due at least partly to factors other than greater glutathione peroxidase and catalase activity in astrocytes. GLIA 33:343–347, 2001. Published 2001 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Astrocytes overexpressing Cu,Zn superoxide dismutase have increased resistance to oxidative injury

Glia, Volume 33 (4) – Mar 15, 2001

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Publisher
Wiley
Copyright
Published 2001 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
D.O.I.
10.1002/1098-1136(20010315)33:4<343::AID-GLIA1033>3.0.CO;2-H
Publisher site
See Article on Publisher Site

Abstract

Overexpression of Cu,Zn SOD (SOD1) can increase survival of neurons under some pathological conditions. Prior studies have shown, however, that SOD1 overexpression can reduce neuronal survival during exposure to superoxide generators by a mechanism involving excess H2O2 accumulation. Since astrocytes exhibit greater H2O2 catabolism capacity than do neurons, the present study examined the effects of SOD1 overexpression on astrocyte survival under these conditions. Cultures were prepared from transgenic mice that overexpress human SOD1 and from nontransgenic littermate controls. Exposure to xanthine oxidase/hypoxanthine (XO/HPX) or menadione caused dose‐dependent astrocyte death. In contrast to prior observations with neurons, astrocytes that overexpress SOD1 showed increased resistance to superoxide toxicity. Surprisingly, increased survival in SOD1 overexpressing cultures remained evident even when H2O2 catabolism was inhibited by preincubation with aminotriazole (to block catalase) and buthionine sulfoximine (to deplete glutathione). These findings suggest differences in superoxide metabolism between neurons and astrocytes, and that the greater resistance of astrocytes to oxidative stress is due at least partly to factors other than greater glutathione peroxidase and catalase activity in astrocytes. GLIA 33:343–347, 2001. Published 2001 Wiley‐Liss, Inc.

Journal

GliaWiley

Published: Mar 15, 2001

References

  • Involvement of glutathione peroxidase and catalase in the disposal of exogenous hydrogen peroxide by cultured astroglial cells
    Dringen, Dringen; Hamprecht, Hamprecht
  • The influence of oxygen free radicals on the permeability of the monolayer of cultured brain endothelial cells
    Imaizumi, Imaizumi; Kondo, Kondo; Deli, Deli; Gobbel, Gobbel; Joó, Joó; Epstein, Epstein; Yoshimoto, Yoshimoto; Chan, Chan
  • Immunochemical detection of metallothionein in brain
    Nakajima, Nakajima; Suzuki, Suzuki

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