Human macrophages limit oxidation products in low density lipoprotein

Hultén, LM; Ullström, C; Krettek, A; Van Reyk, D; Marklund, SL; Dahlgren, C; Wiklund, O

Human macrophages limit oxidation products in low density lipoprotein

Hultén, LM Ullström, C Krettek, A Van Reyk, D

Marklund, SL Dahlgren, C Wiklund, O

Permalink

Publication Type:: Journal Article
Citation:: Lipids in Health and Disease, 2005, 4
Issue Date:: 2005-03-04

Open Access

Copyright Clearance Process

Recently Added
In Progress
Open Access

This item is open access.

Adobe PDF

Download Published VersionAdobe PDF (867.32 kB)

View on publisher's site

View statistics

Full metadata record

Field	Value	Language
dc.contributor.author	Hultén, LM	en_US
dc.contributor.author	Ullström, C	en_US
dc.contributor.author	Krettek, A	en_US
dc.contributor.author	Van Reyk, D https://orcid.org/0000-0002-7768-8662	en_US
dc.contributor.author	Marklund, SL	en_US
dc.contributor.author	Dahlgren, C	en_US
dc.contributor.author	Wiklund, O	en_US
dc.date.available	2005-03-04	en_US
dc.date.issued	2005-03-04	en_US
dc.identifier.citation	Lipids in Health and Disease, 2005, 4	en_US
dc.identifier.issn	1476-511X	en_US
dc.identifier.uri	http://hdl.handle.net/10453/34345
dc.description.abstract	This study tested the hypothesis that human macrophages have the ability to modify oxidation products in LDL and oxidized LDL (oxLDL) via a cellular antioxidant defence system. While many studies have focused on macrophage LDL oxidation in atherosclerosis development, less attention has been given to the cellular antioxidant capacity of these cells. Compared to cell-free controls (6.2 ± 0.7 nmol/mg LDL), macrophages reduced TBARS to 4.42 ± 0.4 nmol/mg LDL after 24 h incubation with LDL (P = 0.022). After 2 h incubation with oxLDL, TBARS were 3.69 ± 0.5 nmol/mg LDL in cell-free media, and 2.48 ± 0.9 nmol/mg LDL in the presence of macrophages (P = 0.034). A reduction of lipid peroxides in LDL (33.7 ± 6.6 nmol/mg LDL) was found in the presence of cells after 24 h compared to cell-free incubation (105.0 ± 14.1 nmol/mg LDL) (P = 0.005). The levels of lipid peroxides in oxLDL were 137.9 ± 59.9 nmol/mg LDL and in cell-free media 242 ± 60.0 nmol/mg LDL (P = 0.012). Similar results were obtained for hydrogen peroxide. Reactive oxygen species were detected in LDL, acetylated LDL, and oxLDL by isoluminol-enhanced chemiluminescence (CL). Interestingly, oxLDL alone gives a high CL signal. Macrophages reduced the CL response in oxLDL by 45% (P = 0.0016). The increased levels of glutathione in oxLDL-treated macrophages were accompanied by enhanced catalase and glutathione peroxidase activities. Our results suggest that macrophages respond to oxidative stress by endogenous antioxidant activity, which is sufficient to decrease reactive oxygen species both in LDL and oxLDL. This may suggest that the antioxidant activity is insufficient during atherosclerosis development. Thus, macrophages may play a dual role in atherogenesis, i.e. both by promoting and limiting LDL-oxidation. © 2005 Hultén et al; licensee BioMed Central Ltd.	en_US
dc.relation.ispartof	Lipids in Health and Disease	en_US
dc.relation.isbasedon	10.1186/1476-511X-4-6	en_US
dc.subject.classification	Nutrition & Dietetics	en_US
dc.subject.mesh	Cells, Cultured	en_US
dc.subject.mesh	Macrophages	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Reactive Oxygen Species	en_US
dc.subject.mesh	Isoenzymes	en_US
dc.subject.mesh	Superoxide Dismutase	en_US
dc.subject.mesh	Lipoproteins, LDL	en_US
dc.subject.mesh	Antioxidants	en_US
dc.subject.mesh	Oxidation-Reduction	en_US
dc.title	Human macrophages limit oxidation products in low density lipoprotein	en_US
dc.type	Journal Article
utslib.citation.volume	4	en_US
utslib.for	0899 Other Information and Computing Sciences	en_US
utslib.for	1101 Medical Biochemistry and Metabolomics	en_US
utslib.for	1111 Nutrition and Dietetics	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	open_access
pubs.publication-status	Published	en_US
pubs.volume	4	en_US

Abstract:

This study tested the hypothesis that human macrophages have the ability to modify oxidation products in LDL and oxidized LDL (oxLDL) via a cellular antioxidant defence system. While many studies have focused on macrophage LDL oxidation in atherosclerosis development, less attention has been given to the cellular antioxidant capacity of these cells. Compared to cell-free controls (6.2 ± 0.7 nmol/mg LDL), macrophages reduced TBARS to 4.42 ± 0.4 nmol/mg LDL after 24 h incubation with LDL (P = 0.022). After 2 h incubation with oxLDL, TBARS were 3.69 ± 0.5 nmol/mg LDL in cell-free media, and 2.48 ± 0.9 nmol/mg LDL in the presence of macrophages (P = 0.034). A reduction of lipid peroxides in LDL (33.7 ± 6.6 nmol/mg LDL) was found in the presence of cells after 24 h compared to cell-free incubation (105.0 ± 14.1 nmol/mg LDL) (P = 0.005). The levels of lipid peroxides in oxLDL were 137.9 ± 59.9 nmol/mg LDL and in cell-free media 242 ± 60.0 nmol/mg LDL (P = 0.012). Similar results were obtained for hydrogen peroxide. Reactive oxygen species were detected in LDL, acetylated LDL, and oxLDL by isoluminol-enhanced chemiluminescence (CL). Interestingly, oxLDL alone gives a high CL signal. Macrophages reduced the CL response in oxLDL by 45% (P = 0.0016). The increased levels of glutathione in oxLDL-treated macrophages were accompanied by enhanced catalase and glutathione peroxidase activities. Our results suggest that macrophages respond to oxidative stress by endogenous antioxidant activity, which is sufficient to decrease reactive oxygen species both in LDL and oxLDL. This may suggest that the antioxidant activity is insufficient during atherosclerosis development. Thus, macrophages may play a dual role in atherogenesis, i.e. both by promoting and limiting LDL-oxidation. © 2005 Hultén et al; licensee BioMed Central Ltd.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/34345