RESUMO
Background: Hypoxia causes oxidative stress and a decrease in osteopontin (OPN) in rats; however, little is known about the change in OPN in lowlander humans during hypobaric hypoxia. We explore the role of the predicted decrease in plasma OPN levels in humans upon high-altitude exposure and its relationship with acute mountain sickness (AMS), as well as superoxide dismutase (SOD) and malondialdehyde (MDA). Methods: Before and during acute altitude exposure, 261 men's plasma OPN, SOD, MDA, heart rate and pulse oximeter saturation (SpO2) were measured. AMS as assessed using the Lake Louise score (LLS) was defined as headache with a total LLS ≥3. Subjects were divided into AMS-0 (non-AMS subjects), mild AMS (headache with total LLS = 3 or 4) and severe AMS groups (headache with total LLS ≥5). Results: At 600 m, no difference in plasma OPN, SOD and MDA was observed between groups. At 3500 m, plasma OPN in severe AMS group was significantly decreased as compared with 600 m. Plasma SOD showed a tendency to decrease during altitude exposure. The opposite trend was observed for plasma MDA. Correlation analysis showed that total LLS was significantly correlated with OPN (ρ = -0.247, P < 0.001) and SOD (ρ = -0.224, P < 0.001). OPN showed significant correlation with SOD (r = 0.235, P < 0.001). Multivariate logistic regression analysis showed that higher plasma OPN was a protective factor for AMS [adjusted odds ratio (OR) 0.924, 95% confidence interval (CI) 0.884-0.966, P < 0.01]. Conclusion: Our results suggest that decreased plasma OPN is correlated with AMS, and oxidative stress may be implicated in this phenomenon. Decreased plasma SOD is also correlated with AMS.
