Androgen treatment of neonatal rats decreases susceptibility of cerebellar granule neurons to oxidative stress in vitro

Androgen treatment of neonatal rats decreases susceptibility of cerebellar granule neurons to... Oxidative stress has been implicated in various neurodegenerative diseases. There is substantial evidence indicating that gonadal hormones can affect neuronal cell survival via both a genomic as well as a non‐genomic mode of action. In the present study, the potential protective activity of testosterone on neuronal cells was investigated by using an in vitro/ex vivo model. Cerebellar granule cells (CGC) were prepared from 7‐day‐old rats which had been treated with a single dose of oil or testosterone propionate on postnatal day 3. After 7 days in culture, cells were exposed to oxidative challenges, including hydrogen peroxide and the nitric oxide donor S‐nitrosocysteine (SNOC), which can induce CGC death via apoptosis. Colchicine, which causes apoptosis via a different mechanism, was also used. The cells were monitored for apoptotic morphology by propidium iodide and TUNEL staining. Additionally, the presence of chromatin fragmentation was determined. CGC obtained from testosterone‐treated rats were found to be more resistant to hydrogen peroxide and nitric oxide toxicity, as shown by a 75 and 45% decrease in apoptotic cells, respectively. In contrast, the susceptibility to colchicine was not modified. As CGC from testosterone‐treated pups were selectively protected from oxidative stress, different components of the antioxidant defence systems were analysed. A twofold increase in the activity of catalase and superoxide dismutase was found in the CGC prepared from testosterone‐treated rats. These results suggest that in vivo treatment with androgens render CGC less vulnerable to oxidative stress‐induced apoptosis by potentiating antioxidant defences. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

Androgen treatment of neonatal rats decreases susceptibility of cerebellar granule neurons to oxidative stress in vitro

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Publisher
Wiley
Copyright
Copyright © 1999 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1046/j.1460-9568.1999.00529.x
Publisher site
See Article on Publisher Site

Abstract

Oxidative stress has been implicated in various neurodegenerative diseases. There is substantial evidence indicating that gonadal hormones can affect neuronal cell survival via both a genomic as well as a non‐genomic mode of action. In the present study, the potential protective activity of testosterone on neuronal cells was investigated by using an in vitro/ex vivo model. Cerebellar granule cells (CGC) were prepared from 7‐day‐old rats which had been treated with a single dose of oil or testosterone propionate on postnatal day 3. After 7 days in culture, cells were exposed to oxidative challenges, including hydrogen peroxide and the nitric oxide donor S‐nitrosocysteine (SNOC), which can induce CGC death via apoptosis. Colchicine, which causes apoptosis via a different mechanism, was also used. The cells were monitored for apoptotic morphology by propidium iodide and TUNEL staining. Additionally, the presence of chromatin fragmentation was determined. CGC obtained from testosterone‐treated rats were found to be more resistant to hydrogen peroxide and nitric oxide toxicity, as shown by a 75 and 45% decrease in apoptotic cells, respectively. In contrast, the susceptibility to colchicine was not modified. As CGC from testosterone‐treated pups were selectively protected from oxidative stress, different components of the antioxidant defence systems were analysed. A twofold increase in the activity of catalase and superoxide dismutase was found in the CGC prepared from testosterone‐treated rats. These results suggest that in vivo treatment with androgens render CGC less vulnerable to oxidative stress‐induced apoptosis by potentiating antioxidant defences.

Journal

European Journal of NeuroscienceWiley

Published: Apr 1, 1999

References

  • Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.
    Gavrieli, Gavrieli; Sherman, Sherman; Ben‐Sasson, Ben‐Sasson
  • Cell death: the significance of apoptosis.
    Wyllie, Wyllie; Kerr, Kerr; Currie, Currie

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