Superoxide anion

metabolite

Superoxide anion inactivates nitric oxide, impairing endothelial vasodilation and promoting inflammation and plaque destabilization.

Pathway placement

Cascade stepPlaque inflammation

Confidencemedium

RationaleOxidative stress mediator; NO inactivation promotes endothelial dysfunction.

Also acts inEndothelial activation/erosion

Druggability

Not assessed (no mapped human gene target).

Type I vs non-Type I discrimination

ScoresShared / rises in both

R — rupture / Type-I

C — non-Type-I

A — assay feasibility

E — evidence strength

T1DI (composite)

Specificity differential (R−C)+4.5

Non-Type-I axis panel

Does this marker also move in each non-Type-I setting? mag 0–3; higher means less Type-I-specific. n/a = no evidence retrieved, which is not the same as no change.

2sepsis / systemic inflammationmag 2

2anemia / acute blood lossmag 2

2hypovolemia / dehydrationn/a

2tachyarrhythmiamag 2

2hypoxemia / respiratory failuren/a

2hypertensive emergencymag 2

2high-demand / peri-operative stressmag 2

3sudden cardiac deathn/a

4aPCI-related periproceduralmag 1

4bstent thrombosisn/a

4cin-stent restenosismag 2

5CABG-relatedmag 2

Coverage: 8/12 axes with evidence

Tier: deep-scored (abstract-extracted) · 18 supporting references. See the discrimination table for all markers.

Assay & specimen

Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.

Specimen

Serum, plasma or urine

Collection tube

Serum separator (gold/red-top, SST) · Lithium heparin (green-top) · Sterile urine container

Method / principle

LC-MS/MS (targeted metabolomics) or enzymatic colorimetric where available

Reagent / substrate

Stable-isotope-labeled internal standard (MS); or enzyme-coupled Trinder reagent

Platform

LC-MS/MS; some automated chemistry

Turnaround · availability

Send-out / research · Specialized / research

Literature evidence(1)

Atherosclerosis-associated endothelial dysfunction.
Zeitschrift fur Kardiologie · 2000 · PMID 11151799 · doi