Circulating levels of selenium-binding protein 1 (SELENBP1) are associated with risk for major adverse cardiac events and death

Abstract

ObjectiveSelenium-binding protein 1 (SELENBP1) is an intracellular protein with variable expression in response to cellular stress. As the selenium (Se) status is affected by inflammation and hypoxia, we hypothesized that SELENBP1 contributes to disease-specific Se metabolism. To test this hypothesis, a quantitative assay was developed and used to monitor SELENBP1 in patients with acute coronary syndrome (ACS). Materials and methodsSELENBP1 was expressed, antibodies were generated and a luminometric immuno assay (LIA) was established and characterized. Serum samples were collected from controls (n = 37) and patients (n = 85) admitted to the Chest Pain Unit with suspected ACS. Blood samples were available from time of first medical contact in the ambulance, at admission to hospital, and after 2, 4, 6 and 12–36 h. ResultsCirculating SELENBP1 was close to limit of detection in healthy controls and elevated in patients with suspected ACS. SELENBP1 was unrelated to other biomarkers of myocardial damage such as troponin T or aspartate aminotransferase. Serum SELENBP1 enabled a categorization of patients on first medical contact as either high-risk or low-risk for major adverse cardiac events (MACE) or death, when using 0.8 nmol/l as threshold. The odds-ratios (OR) for MACE and death were OR = 11 (95% CI: 2–49, p = 0.0022) and OR = 12 (2–74, p = 0.014), respectively. ConclusionsUntil now, SELENBP1 was mainly considered as an intracellular protein involved in Se metabolism and redox control. Our data indicate that SELENBP1 constitutes a circulating biomarker for cardiac events categorizing patients with suspected ACS at first medical contact into high-risk or low-risk for MACE and death, independent from and complimentary to current biomarkers.