Escherichia coli endotoxin-mediated endothelial injury is modulated by glutathione ethyl ester

Peter E. Morris, Arthur P. Wheeler, Barbara O. Meyrick, Gordon R. Bernard

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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.

Original languageEnglish
Pages (from-to)1119-1122
Number of pages4
JournalJournal of Infectious Diseases
Issue number4
StatePublished - Oct 1995

ASJC Scopus subject areas

  • General Medicine


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