Depressed serum selenoprotein P: possible new predicator of increased risk for cerebrovascular events

Selenium protection against cellular damage by oxygen radicals is accomplished through selenoproteins. Thus, selenium protection during the development of stroke, an oxidative stress–related disease, may not be appropriately reflected in the total serum selenium concentration. Therefore, we hypothesized that serum selenoproteins should also be measured to understand the relationship between selenium status and oxidative stress. To establish whether stroke is associated with changes in serum selenoprotein levels, a population-based, nested case-control study was performed. The subjects were recruited from 1632 residents older than 40 years who had completed health examinations in 1992. Blood samples collected from 30 controls and 30 initial stroke victims between 1992 and 1994 were analyzed for total serum selenium and selenium-containing protein distribution. Selenium-containing proteins were separated using 2 high-performance liquid chromatography columns in tandem and detected by inductively coupled plasma–mass spectrometry. The mean serum selenium concentration was lower in the patients who had a stroke than in the controls (105.2 vs 116.5 μg/L). Selenium contents in glutathione peroxidase and albumin did not show any significant difference; however, selenoprotein P was significantly lower in the stroke cases than in the controls (54.5 vs 63.0 μg/L, P = .006). Results from multivariate logistic regression analysis showed that reduced serum level of selenoprotein P was associated with a higher risk of stroke (odds ratio = 0.28; 95% confidence interval, 0.10-0.85).