Enhancement of NO release from S-nitrosoalbumin by pollution derived metal ions.

S-Nitrosothiols act as a comparatively long-lived reservoir of releasable nitric oxide (NO) present in vivo in a variety of body fluids. Soluble constituents of air-borne particulate matter (PM) can affect S-nitrosothiol stability and deregulate NO-based biological signaling. PM aqueous extracts of standard urban dust (SRM 1648a) were prepared, and their effect on human serum S-nitrosoalbumin (HSA-NO) stability was studied. The results indicated that PM extracts induced a release of NO from HSA-NO in a dose-dependent manner. To identify the inorganic components of urban PM responsible for HSA-NO decomposition, the effects of individual metal ions and metal ion mixtures, detected in the SRM 1648a aqueous extract, were examined. The dominant role of copper ions (specifically Cu+) was confirmed, but the results did not exclude the influence of other water-soluble PM components. Measurements with the application of several common metal ion chelators confirmed that Cu2+ may participate in NO release from HSA-NO and that reduction to monovalent Cu+ (responsible for S-NO bond breaking) may occur with the participation of S-nitrosoalbumin. The addition of ascorbic acid (AscA) significantly enhanced the effectiveness of NO release by PM extracts both kinetically and quantitatively, by inducing an increase in the reduction of Cu2+ to Cu+. These results indicate that AscA present in the respiratory tract lining fluids and plasma may amplify the activity of inorganic components of PM in S-nitrosothiol decomposition.