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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1367.)
© 2002 American Heart Association, Inc.

Editorials

Toward Understanding of Extracellular Superoxide Dismutase Regulation in Atherosclerosis

A Novel Role of Uric Acid?

Ulf Landmesser; Helmut Drexler

From the Abteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Germany.

Correspondence to Helmut Drexler, MD, Medizinische Hochschule Hannover, Abteilung Kardiologie und Angiologie, Carl Neuberg Str 1, 30625 Hannover, Germany. E-mail Drexler.Helmut@MH-Hannover.de

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Superoxide dismutases (SODs) represent the major antioxidant defense system against superoxide anions (O₂^·-). Three isoforms of superoxide dismutase have been identified in mammals: copper-zinc SOD (Cu, Zn-SOD), manganese SOD (Mn-SOD), and extracellular SOD (ecSOD). Cu, Zn- and Mn-SOD are localized intracellularly, whereas the last discovered SOD isoform, ecSOD,¹ is secreted and bound to heparan sulfate on the cellular surface.

See page 1402

The arterial wall contains exceptionally large amounts of ecSOD in the interstitium that are about 100 times higher compared with other tissues such as muscle or fat tissue, suggesting a special function of this SOD isoform within the vascular wall.^2,3 In some human vessels, ecSOD accounts for more than 70% of total SOD activity.^2,3 An important function of ecSOD in the arterial wall may be the preservation of bioactivity of nitric oxide(NO^·) with its antiatherogenic and vasodilating effects. NO^· reacts at an almost diffusion-controlled rate with O₂^·- resulting in loss of NO^· bioactivity (estimated rate constant: 6.7x10⁹ M^-1/s^-1).⁴ ecSOD degrades O₂^·- at an estimated rate of 4x10⁹ M^-1/s^-1, ¹ that is 4 to 5 orders of magnitude faster than antioxidants such as vitamin C or E⁵ and may therefore be particularly effective in protecting NO^· from inactivation by O₂^·-. Indeed, studies using rabbit aortas or bovine coronary arteries have shown that inhibition of vascular SOD activity results in a rapid impairment of endothelium-dependent, NO^·-mediated vasodilation, suggesting that SOD levels are critical for the ability of NO^· to . . . [Full Text of this Article]

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