Cited by 199Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressSelenium in Biological Systems

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Cellular glutathione peroxidase deficiency and endothelial dysfunction

Forgione, Marc A., Weiss, Norbert, Heydrick, Stanley, Cap, André, Klings, Elizabeth S., Bierl, Charlene, Eberhardt, Robert T., Farber, Harrison W., Loscalzo, Joseph·2002·American Journal of Physiology-Heart and Circulatory Physiology

DOI 10.1152/ajpheart.00598.2001

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Abstract

Cellular glutathione peroxidase (GPx-1) is the most abundant intracellular isoform of the GPx antioxidant enzyme family. In this study, we hypothesized that GPx-1 deficiency directly induces an increase in vascular oxidant stress, with resulting endothelial dysfunction. We studied vascular function in a murine model of homozygous deficiency of GPx-1 (GPx-1−/−). Mesenteric arterioles of GPx-1−/−mice demonstrated paradoxical vasoconstriction to β-methacholine and bradykinin, whereas wild-type (WT) mice showed dose-dependent vasodilation in response to both agonists. One week of treatment of GPx-1−/−mice withl-2-oxothiazolidine-4-carboxylic acid (OTC), which increases intracellular thiol pools, resulted in restoration of normal vascular reactivity in the mesenteric bed of GPx-1−/−mice. We observed an increase of the isoprostane iPF 2α-III, a marker of oxidant stress, in the plasma and aortas of GPx-1−/−mice compared with WT mice, which returned toward normal after OTC treatment. Aortic sections from GPx-1−/−mice showed increased binding of an anti-3-nitrotyrosine antibody in the absence of frank vascular lesions. These findings demonstrate that homozygous deficiency of GPx-1 leads to impaired endothelium-dependent vasodilator function presumably due to a decrease in bioavailable nitric oxide and to increased vascular oxidant stress. These vascular abnormalities can be attenuated by increasing bioavailable intracellular thiol pools.

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Authors: Forgione, M. A., Weiss, N., Heydrick, S., Cap, A., Klings, E. S., Bierl, C., Eberhardt, R. T., Farber, H. W., & Loscalzo, J.
Affiliations: Evans Department of Medicine,
Whitaker Cardiovascular Institute, Department of Pharmacology, and
Boston University (US)
ORCID: Weiss, Norbert
Klings, Elizabeth S.
Eberhardt, Robert T.
Farber, Harrison W.
Loscalzo, Joseph
Venue: American Journal of Physiology-Heart and Circulatory Physiology
Publisher: American Physiological Society
Published: 2002-04-01
Volume: 282
Issue: 4
Pages: H1255-H1261
ISSN: 0363-6135 (ISSN-L)
1522-1539
DOI: 10.1152/ajpheart.00598.2001
OpenAlex: W2139527140
Cited by: 199
References: 41
Citations by year: 2026: 4 · 2025: 12 · 2024: 3 · 2023: 8 · 2022: 7 · 2021: 11 · 2020: 5 · 2019: 10 · 2018: 3 · 2017: 9 · 2016: 10 · 2015: 6 · 2014: 9 · 2013: 9 · 2012: 10
FWCI: 4.80
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (HL61795, HL 55993, HL-07224-24, HL58976, R01HL058976, T32HL007224, P50HL055993)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
Keywords: glutathione peroxidase 1, endothelial dysfunction, mesenteric arterioles, endothelium-dependent vasodilation, nitric oxide bioavailability, nitrotyrosine, L-2-oxothiazolidine-4-carboxylic acid, bradykinin, aorta
MeSH terms: Animals, Bradykinin, Endothelium, Vascular, Glutathione Peroxidase, Cyclic GMP, Microcirculation, Nitroprusside, Splanchnic Circulation, Methacholine Chloride, Mice, Knockout, Oxidative Stress, Nitric Oxide Synthase, Models, Animal, Mice, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III

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