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We measured the accumulation of 4-hydroxynonenal (HNE), a major lipid peroxidation product during hypoxia/reoxygenation of brain capillary endothelial cells (BCEC). The concentration of HNE after 2 h of hypoxia was 0.23 nmol/mg protein and rose up to 0.28 nmol/mg protein after 30 min of reoxygenation. That reflects a 1.5-fold increase, whereas aortic endothelial cells (AEC) increased the HNE level 5-fold, compared to the control. Therefore, the ability of BCEC to degrade exogenously added HNE was tested. The HNE consumption in BCEC achieved a rate of about 600 nmol.min-1.mg protein-1, about two times higher than in AEC. The higher ability of BCEC to degrade HNE is probably the reason of the 2-fold higher IC50 value against the aldehyde. Therefore, we concluded that the high ability of BCEC to degrade HNE is a substantial part of the secondary antioxidative defense of the brain.
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