Protective activity of propofol, Diprivan® and intralipid against active oxygen species

We separately studied the antioxidant properties of propofol (PPF), Diprivan® (the commercial form of PPF) and intralipid (IL) (the vehicle solution of PPF in Diprivan® ) on active oxygen species produced by phorbol myristate acetate (10-6M)-stimulated human polymorphonuclear leukocytes (PMN: 5 × 10...

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Main Authors: M. Mathy-Hartert, G. Deby-Dupont, P. Hans, C. Deby, M. Lamy
Format: Article
Language:English
Published: Wiley 1998-01-01
Series:Mediators of Inflammation
Subjects:
Online Access:http://dx.doi.org/10.1080/09629359890848
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author M. Mathy-Hartert
G. Deby-Dupont
P. Hans
C. Deby
M. Lamy
author_facet M. Mathy-Hartert
G. Deby-Dupont
P. Hans
C. Deby
M. Lamy
author_sort M. Mathy-Hartert
collection DOAJ
description We separately studied the antioxidant properties of propofol (PPF), Diprivan® (the commercial form of PPF) and intralipid (IL) (the vehicle solution of PPF in Diprivan® ) on active oxygen species produced by phorbol myristate acetate (10-6M)-stimulated human polymorphonuclear leukocytes (PMN: 5 × 10 5 cells/ assay), human endothelial cells (5 × 105 cells/assay) or cell-free systems (NaOCl or H2O2/peroxidase systems), using luminol (10-4M)-enhanced chemiluminescence (CL). We also studied the protective effects of Diprivan® on endothelial cells submitted to an oxidant stress induced by H2O2/MPO system: cytotoxicity was assessed by the release of preincorporated 51Cr. Propofol inhibited the CL produced by stimulated PMN in a dose dependent m anner (until 5 × 10-5 M, a clinically relevant concentration), while Diprivan® and IL were not dose-dependent inhibitors. The CL produced by endothelial cells was dosedependently inhibited by Diprivan® and PPF, and weakly by IL (not dose-dependent). In cell free systems, dose-dependent inhibitions were obtained for the three products with a lower effect for IL. Diprivan® efficaciously protected endothelial cells submitted to an oxidant stress, while IL was ineffective. By HPLC, we demonstrated that PPF was not incorporated into the cells. The drug thus acted by scavenging the active oxygen species released in the extracellular medium. IL acted in the same manner, but was a less powerful antioxidant.
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spelling doaj-art-7e9773bde95744d5ab57f107c4152f042025-02-03T06:07:29ZengWileyMediators of Inflammation0962-93511466-18611998-01-017532733310.1080/09629359890848Protective activity of propofol, Diprivan® and intralipid against active oxygen speciesM. Mathy-Hartert0G. Deby-Dupont1P. Hans2C. Deby3M. Lamy4Centre for the Biochemistry of Oxygen, Institut de Chimie, B6a, Domaine Universitaire du Sart Tilman, Liège 4000, BelgiumCentre for the Biochemistry of Oxygen, Institut de Chimie, B6a, Domaine Universitaire du Sart Tilman, Liège 4000, BelgiumDepartment of Anaesthesiology and Intensive Care, Centre Hospitalier Universitaire, B35, Domaine Universitaire du Sart Tilman, Liège 4000, BelgiumCentre for the Biochemistry of Oxygen, Institut de Chimie, B6a, Domaine Universitaire du Sart Tilman, Liège 4000, BelgiumCentre for the Biochemistry of Oxygen, Institut de Chimie, B6a, Domaine Universitaire du Sart Tilman, Liège 4000, BelgiumWe separately studied the antioxidant properties of propofol (PPF), Diprivan® (the commercial form of PPF) and intralipid (IL) (the vehicle solution of PPF in Diprivan® ) on active oxygen species produced by phorbol myristate acetate (10-6M)-stimulated human polymorphonuclear leukocytes (PMN: 5 × 10 5 cells/ assay), human endothelial cells (5 × 105 cells/assay) or cell-free systems (NaOCl or H2O2/peroxidase systems), using luminol (10-4M)-enhanced chemiluminescence (CL). We also studied the protective effects of Diprivan® on endothelial cells submitted to an oxidant stress induced by H2O2/MPO system: cytotoxicity was assessed by the release of preincorporated 51Cr. Propofol inhibited the CL produced by stimulated PMN in a dose dependent m anner (until 5 × 10-5 M, a clinically relevant concentration), while Diprivan® and IL were not dose-dependent inhibitors. The CL produced by endothelial cells was dosedependently inhibited by Diprivan® and PPF, and weakly by IL (not dose-dependent). In cell free systems, dose-dependent inhibitions were obtained for the three products with a lower effect for IL. Diprivan® efficaciously protected endothelial cells submitted to an oxidant stress, while IL was ineffective. By HPLC, we demonstrated that PPF was not incorporated into the cells. The drug thus acted by scavenging the active oxygen species released in the extracellular medium. IL acted in the same manner, but was a less powerful antioxidant.http://dx.doi.org/10.1080/09629359890848Active ox ygen speciesPropofolDiprivan®IntralipidPolymorphonuclear neutrophilsEndothelial cells.
spellingShingle M. Mathy-Hartert
G. Deby-Dupont
P. Hans
C. Deby
M. Lamy
Protective activity of propofol, Diprivan® and intralipid against active oxygen species
Mediators of Inflammation
Active ox ygen species
Propofol
Diprivan®
Intralipid
Polymorphonuclear neutrophils
Endothelial cells.
title Protective activity of propofol, Diprivan® and intralipid against active oxygen species
title_full Protective activity of propofol, Diprivan® and intralipid against active oxygen species
title_fullStr Protective activity of propofol, Diprivan® and intralipid against active oxygen species
title_full_unstemmed Protective activity of propofol, Diprivan® and intralipid against active oxygen species
title_short Protective activity of propofol, Diprivan® and intralipid against active oxygen species
title_sort protective activity of propofol diprivan r and intralipid against active oxygen species
topic Active ox ygen species
Propofol
Diprivan®
Intralipid
Polymorphonuclear neutrophils
Endothelial cells.
url http://dx.doi.org/10.1080/09629359890848
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