TY - JOUR
T1 - Escherichia coli endotoxin-mediated endothelial injury is modulated by glutathione ethyl ester
AU - Morris, Peter E.
AU - Wheeler, Arthur P.
AU - Meyrick, Barbara O.
AU - Bernard, Gordon R.
PY - 1995/10
Y1 - 1995/10
N2 - The mechanisms involved in endotoxin-induced endothelial injury are not fully understood. Oxidant stress is thought to play a role in cell damage after endotoxin exposure. Glutathione may ameliorate these affects. Glutathione ethyl ester(GSE) was used in bovine pulmonary artery endothelial cell (BPAEC) cultures to determine the potential for attenuation of endotoxin-induced injury. GSE (0.05–25 mM) was preincubated with BPAEC for 4 h before endotoxin exposure. Fresh media containing GSE and Escherichia coli endotoxin (0.05 μg/mL) were then placed on the BPAEC and incubated for 18 h. GSE, at doses of 5 and 25 ro M, attenuated endotoxin-induced injury, as reflected by a significant reduction in lactate dehydrogenase release. This was paralleled by a significant increase in endotoxin-stimulated prostaglandin E2and prostacyclin release. Thus, GSE attenuates endotoxin-induced injury of BPAEC in culture and alters BPAEC prostaglandin metabolism.
AB - The mechanisms involved in endotoxin-induced endothelial injury are not fully understood. Oxidant stress is thought to play a role in cell damage after endotoxin exposure. Glutathione may ameliorate these affects. Glutathione ethyl ester(GSE) was used in bovine pulmonary artery endothelial cell (BPAEC) cultures to determine the potential for attenuation of endotoxin-induced injury. GSE (0.05–25 mM) was preincubated with BPAEC for 4 h before endotoxin exposure. Fresh media containing GSE and Escherichia coli endotoxin (0.05 μg/mL) were then placed on the BPAEC and incubated for 18 h. GSE, at doses of 5 and 25 ro M, attenuated endotoxin-induced injury, as reflected by a significant reduction in lactate dehydrogenase release. This was paralleled by a significant increase in endotoxin-stimulated prostaglandin E2and prostacyclin release. Thus, GSE attenuates endotoxin-induced injury of BPAEC in culture and alters BPAEC prostaglandin metabolism.
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U2 - 10.1093/infdis/172.4.1119
DO - 10.1093/infdis/172.4.1119
M3 - Article
C2 - 7561193
AN - SCOPUS:0029119420
SN - 0022-1899
VL - 172
SP - 1119
EP - 1122
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 4
ER -