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1 Institute for Environmental Medicine, and Departments of 2 Emergency Medicine and 3 Biochemistry and Biophysics, The University of Pennsylvania, Philadelphia, Pennsylvania 19104-6068
Received 8 December 1995; accepted in final form 18 December 1996.
Thom, Stephen R., Melissa Kang, Donald Fisher, and Harry
Ischiropoulos. Release of glutathione from erythrocytes and other
markers of oxidative stress in carbon monoxide poisoning. J. Appl. Physiol. 82(5):
1424-1432, 1997.
Rats exposed to CO in a manner known to cause
oxidative stress in brain exhibited a twofold increase in plasma levels
of oxidized proteins, thiobarbituric acid-reactive substances (TBARS),
oxidized glutathione (GSSG), and reduced glutathione
(GSH). Changes were neither directly related to hypoxic
stress from carboxyhemoglobin nor significantly influenced by
circulating platelets or neutrophils. Treatment with the nitric oxide
synthase inhibitor
N
-nitro-L-arginine methyl
ester inhibited elevations in GSH and GSSG but not changes
in oxidized proteins or TBARS, suggesting that two oxidative mechanisms
may be operating in this model and that GSH and GSSG elevations
involved nitric oxide-derived oxidants. Elevations of blood GSH and
GSSG occurred at different anatomic sites, indicating that no single
organ was the source of the increased peptides. Animals that underwent
exchange transfusion with a hemoglobin-containing saline solution did
not exhibit elevations in GSH and GSSG, suggesting that blood-borne
cells released these peptides in response to oxidative stress. In in
vitro studies, erythrocytes, but not platelets and leukocytes,
responded to oxidative stress from peroxynitrite by releasing GSH,
whereas no release was observed in response to nitric oxide or
superoxide. Glucose, maltose, and cytochalasin B, agents that protect
extracellular components of the hexose transport protein complex from
oxidative stress, prevented GSH release. The data indicate that nitric
oxide-derived oxidants are involved in CO-mediated oxidative stress
within the vascular compartment and that elevations of several
compounds may be useful for identifying exposures to CO likely to
precipitate brain injury.
peroxynitrite; nitric oxide; oxidized proteins; thiobarbituric acid reactive substances; hexose transport
This article has been cited by other articles:
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  S. R. Thom, D. Fisher, and Y. Manevich Roles for platelet-activating factor and {middle dot}NO-derived oxidants causing neutrophil adherence after CO poisoning Am J Physiol Heart Circ Physiol, August 1, 2001; 281(2): H923 - H930. [Abstract] [Full Text] [PDF]
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 J. J. E. Haddad, B. Safieh-Garabedian, N. E. Saadé, and S. C. Land Thiol Regulation of Pro-Inflammatory Cytokines Reveals a Novel Immunopharmacological Potential of Glutathione in the Alveolar Epithelium J. Pharmacol. Exp. Ther., March 1, 2001; 296(3): 996 - 1005. [Abstract] [Full Text]
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 S. R. Thom, D. Fisher, Y. A. Xu, K. Notarfrancesco, and H. Ischiropoulos Adaptive responses and apoptosis in endothelial cells exposed to carbon monoxide PNAS, February 1, 2000; 97(3): 1305 - 1310. [Abstract] [Full Text] [PDF]
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S. R. Thom, D. Fisher, Y. A. Xu, S. Garner, and H. Ischiropoulos Role of nitric oxide-derived oxidants in vascular injury from carbon monoxide in the rat Am J Physiol Heart Circ Physiol, March 1, 1999; 276(3): H984 - H992. [Abstract] [Full Text] [PDF]
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