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Originally published In Press as doi:10.1194/jlr.M500377-JLR200 on February 28, 2006

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Journal of Lipid Research, Vol. 47, 1157-1167, June 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology

Lack of the antioxidant glutathione peroxidase-1 does not increase atherosclerosis in C57BL/J6 mice fed a high-fat diet

Judy B. de Haan1,*,{dagger}, Paul K. Witting§,**, Nada Stefanovic*, Josefa Pete{dagger}{dagger}, Michael Daskalakis§§, Ismail Kola***, Roland Stocker2,§ and Joseph J. Smolich2,{dagger}{dagger}{dagger}

* Oxidative Stress Group, Baker Heart Research Institute, Melbourne, Australia
{dagger} Monash Institute of Medical Research, Monash University, Melbourne, Australia
§ Centre for Vascular Research, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia
** Vascular Biology Group, ANZAC Research Institute, Concord Repatriation General Hospital, Concord, New South Wales, Australia
{dagger}{dagger} Diabetic Complications Group, Baker Heart Research Institute, Melbourne, Australia
§§ Southern Cross Pathology Australia, Monash Medical Centre, Melbourne, Australia
*** Merck Research Laboratories, Merck & Co., Inc., Rahway, NJ
{dagger}{dagger}{dagger} Centre for Heart and Chest Research, Monash University Department of Medicine, Monash Medical Centre, Melbourne, Australia

Published, JLR Papers in Press, February 28, 2006.

2 R. Stocker and J. J. Smolich contributed equally to this work.

1 To whom correspondence should be addressed. e-mail: judy.dehaan{at}baker.edu.au

Oxidative stress is thought to contribute to the initiation and progression of atherosclerosis. As glutathione peroxidase-1 (Gpx1) is an antioxidant enzyme that detoxifies lipid hydroperoxides, we tested the impact of Gpx1 deficiency on atherosclerotic processes and antioxidant enzyme expression in mice fed a high-fat diet (HFD). After 12 weeks of HFD, atherosclerotic lesions at the aortic sinus were of similar size in control and Gpx1-deficient mice. However, after 20 weeks of HFD, lesion size increased further in control but not in Gpx1-deficient mice, even though plasma and aortic wall markers of oxidative damage did not differ between groups. In control mice, the expression of Gpx1 increased and that of Gpx3 decreased at the aortic sinus after 20 weeks of HFD, with no change in the expression of Gpx2, Gpx4, catalase, peroxiredoxin-6, glutaredoxin-1 and -2, or thioredoxin-1 and -2. By comparison, in Gpx1-deficient mice, the expression of antioxidant genes was unaltered except for a decrease in glutaredoxin-1 and an increase in glutaredoxin-2. These changes were associated with increased expression of the proinflammatory marker monocyte chemoattractant protein-1 in control mice but not in Gpx1-deficient mice. In summary, a specific deficiency in Gpx1 was not accompanied by an increase in markers of oxidative damage or increased atherosclerosis in a murine model of HFD-induced atherogenesis.

Supplementary key words antioxidant enzymes • lipid hydroperoxides • knockout mice • oxidative stress


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