Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
This Article
Right arrow Order Full text via Infotrieve
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rosenbaum, D. M.
Right arrow Articles by Kessler, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rosenbaum, D. M.
Right arrow Articles by Kessler, J. A.
Right arrowPubmed/NCBI databases
*Substance via MeSH

Stroke, Vol 25, 857-862, Copyright © 1994 by American Heart Association


ARTICLES

Superoxide dismutase ameliorates neuronal death from hypoxia in culture

DM Rosenbaum, J Kalberg and JA Kessler
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461.

BACKGROUND AND PURPOSE: Studies showing efficacy with free radical scavengers have been conflicting, and when protection was demonstrated it was attributed to action at the level of the vascular endothelium. The purpose of this study was to test the hypotheses that neuronal free radical formation plays a role in the ischemic cascade and occurs intracellularly and that free radical scavengers, if taken up intracellularly, will protect against hypoxic damage. METHODS: A tissue culture model of hypoxia followed by restoration of oxygen was employed, using both superior cervical ganglia and hippocampal neurons. Cells were exposed to an anoxic atmosphere of 95% N2 and 5% CO2 and examined 2 to 24 hours later after restoration of oxygen. Determination of survival was measured by trypan blue exclusion. Nitroblue tetrazolium stain was used to assess free radical formation. RESULTS: Pretreatment with free superoxide dismutase did not decrease cell death after hypoxia as measured by trypan blue exclusion. However, when superoxide dismutase was taken up intracellularly under depolarizing conditions (55 mmol/L KCl in the medium), cell death was decreased significantly compared with hypoxic controls (28.7 +/- 4.34 versus 40.3 +/- 4.33; P < .03). During hypoxia neurons reduced nitroblue tetrazolium to form the blue precipitate formazan, and the color change was blocked in neurons pretreated with superoxide dismutase in depolarizing medium. Similar findings occurred in both superior cervical ganglia and hippocampal neurons. CONCLUSIONS: These findings provide evidence to support the role of neuronal free radical formation in cell death secondary to hypoxia. In addition, free radical scavengers, if taken up intracellularly, may partially ameliorate their deleterious effect.


This article has been cited by other articles:


Home page
J. Thorac. Cardiovasc. Surg.Home page
N. Yoshimura, M. Okada, T. Ota, and H. Nohara
Pharmacologic intervention for ischemic brain edema after retrograde cerebral perfusion
J. Thorac. Cardiovasc. Surg., June 1, 1995; 109(6): 1173 - 1181.
[Abstract] [Full Text]


Home page
ScienceHome page
C. Thompson
Apoptosis in the pathogenesis and treatment of disease
Science, March 10, 1995; 267(5203): 1456 - 1462.
[Abstract] [PDF]