Catalysis of S-nitrosothiols Formation by Serum Albumin: The Mechanism and Implication in Vascular Control

Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):5913-8. doi: 10.1073/pnas.092048999.

Abstract

Nitric oxide (NO(.)) is a short-lived physiological messenger. Its various biological activities can be preserved in a more stable form of S-nitrosothiols (RS-NO). Here we demonstrate that at physiological NO(.) concentrations, plasma albumin becomes saturated with NO(.) and accelerates formation of low-molecular-weight (LMW) RS-NO in vitro and in vivo. The mechanism involves micellar catalysis of NO(.) oxidation in the albumin hydrophobic core and specific transfer of NO(+) to LMW thiols. Albumin-mediated S-nitrosylation and its vasodilatory effect directly depend on the concentration of circulating LMW thiols. Results suggest that the hydrophobic phase formed by albumin serves as a major reservoir of NO(.) and its reactive oxides and controls the dynamics of NO(.)-dependant processes in the vasculature.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Albumins / metabolism
  • Animals
  • Catalysis*
  • Dose-Response Relationship, Drug
  • Femoral Artery / metabolism*
  • Femoral Vein / metabolism*
  • Male
  • Micelles
  • Models, Biological
  • Nitric Oxide / chemistry
  • Nitric Oxide / metabolism*
  • Nitrites / metabolism
  • Rats
  • Rats, Wistar
  • S-Nitrosothiols / metabolism*
  • Sulfhydryl Compounds / metabolism
  • Time Factors
  • Water / chemistry

Substances

  • Albumins
  • Micelles
  • Nitrites
  • S-Nitrosothiols
  • Sulfhydryl Compounds
  • Water
  • Nitric Oxide