Plasma Glutathione and Glutathione Disulfide Levels in the Rat when Subjected to Combinations of Endotoxins, Hepatic lschemiaReperfusion, Cecal Ligation and Puncture, and Complement Activation
Loading...
Authors
Michaels, Anothony J. (Tony)
Issue Date
1996
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
The main purpose of this study was to set up different models that would
produce various levels of oxidative stress. The oxidative stress was measured in
male Fischer and Sprague-Dawley rats subjected to a variety of insults through
glutathione disulfide (GSSG) levels that were monitored intracellularly (tissue
samples) and extracellularly (plasma samples). Glutathione levels were
measured after injections of paraquat and endotoxin (Salmonella entertidis,
Salmonella abortus equi and E. coli), and after 45 min hepatic ischemia
followed by 2 h reperfusion combined with cecal ligation and puncture (CLP) ,
endotoxin, or saline. Complement activation was also observed with cobra
venom factor (CVF), and with CVF + CLP. The greatest stress was seen in the
animals that were subjected to insults of 45 min ischemia + 2 h reperfusion + 1
µg/kg S. entertidis. The percentage of GSSG observed in the plasma was as
high as 66%. The animals that were subjected only to insults of endotoxin did
not show a higher stress than the ischemia animals, but oxidative stress was
definitely occurring. The highest percentage of oxidized glutathione in the
plasma was seen when the animals were given injections of 60 mg/kg of the
redox-cycling agent paraquat. The GSSG percentage in the plasma was as high
as 55% with animals subjected to paraquat.
The results did not show much evidence for intracellular oxidative
stress occurring. The livers and lungs isolated from the animals after the
endotoxemia experiments showed a less than 1% oxidative glutathione in the
tissue. Therefore, the majority of the results demonstrate a priming of
Kupffer cells and neutrophils for reactive oxygen production occurring
mainlyextracellularly. A greater stress causes a greater build up of oxygen
radicals, causing an increase in GSSG as it becomes oxidized from GSH. These
results may further help the scientific community to fight the excessive
inflammatory response often seen after major traumas.
Description
vi, 36 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.