Antioxidant enzyme deficiencies and vascular disease

Abstract

Cellular respiration in an oxygen-rich environment leads to the generation of reactive oxygen species. These partially reduced forms of molecular oxygen can readily react with biological molecules, often modifying their normal biological function. Antioxidant enzyme mechanisms have evolved to eliminate reactive oxygen species and minimize the oxidant stress caused by their reactivity. Inherited and acquired deficiencies of key antioxidant enzymes lead to a dysregulated redox environment, which can promote pathobiology; when this redox dysfunction occurs in the blood vessel, vascular disease ensues. In this article, we consider three distinct antioxidant enzyme deficiencies – glucose-6-phosphate dehydrogenase, glutathione peroxidase-1 and glutathione peroxidase-3 – and their consequences for vascular disease.

Keywords::

• endothelial function
• glutathione
• nitric oxide
• oxygen
• superoxide

Acknowledgements

Joseph Loscalzo wishes to acknowledge Ms Stephanie Tribuna for expert secretarial assistance.

Financial & competing interests disclosure

This work was supported in part by NIH grants HL61795, HL81587, HL70929 and HV28178. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.