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Related Experiment Videos

Cellular glutathione peroxidase deficiency and endothelial dysfunction.

Marc A Forgione1, Norbert Weiss, Stanley Heydrick

  • 1Evans Department of Medicine, Boston, Massachusetts 02118, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|March 15, 2002
PubMed
Summary

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Cellular glutathione peroxidase (GPx-1) deficiency causes vascular oxidant stress and endothelial dysfunction. Restoring intracellular thiols with L-2-oxothiazolidine-4-carboxylic acid (OTC) improved vascular reactivity in GPx-1 deficient mice.

Area of Science:

  • Biochemistry
  • Physiology
  • Cardiovascular Research

Background:

  • Cellular glutathione peroxidase (GPx-1) is a key intracellular antioxidant enzyme.
  • GPx-1 deficiency is hypothesized to increase vascular oxidant stress and impair endothelial function.
  • Understanding GPx-1's role is crucial for cardiovascular health and antioxidant defense.

Purpose of the Study:

  • To investigate the direct impact of GPx-1 deficiency on vascular function and oxidant stress.
  • To determine if enhancing intracellular thiol pools can ameliorate GPx-1 deficiency-induced vascular abnormalities.

Main Methods:

  • Utilized a murine model of homozygous GPx-1 deficiency (GPx-1(-/-)) and wild-type (WT) controls.
  • Assessed vascular reactivity in mesenteric arterioles using agonists like beta-methacholine and bradykinin.

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  • Measured plasma and aortic isoprostane levels (iPF(2alpha)-III) as markers of oxidant stress.
  • Evaluated aortic sections for nitrotyrosine adducts.

    • Main Results:

    • GPx-1(-/-) mice exhibited paradoxical vasoconstriction to agonists, unlike WT mice which showed vasodilation.
    • Increased levels of the oxidant stress marker iPF(2alpha)-III were found in GPx-1(-/-) mice.
    • Treatment with L-2-oxothiazolidine-4-carboxylic acid (OTC) restored normal vascular reactivity in GPx-1(-/-) mice.
    • OTC treatment also reduced iPF(2alpha)-III levels towards normal.

    Conclusions:

    • Homozygous GPx-1 deficiency impairs endothelium-dependent vasodilation, likely due to reduced nitric oxide bioavailability and increased vascular oxidant stress.
    • Increased vascular oxidant stress in GPx-1 deficiency is evidenced by elevated iPF(2alpha)-III and nitrotyrosine.
    • Augmenting intracellular thiol pools with OTC can effectively attenuate these vascular abnormalities.