Related Experiment Video
Updated: Jun 4, 2026

En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Oxidative stress impairs endothelial nitric oxide levels in Behçets' disease
Ece Onur1, Ceyda Kabaroglu, Isil Inanir
1Celal Bayar University School of Medicine, Department of Biochemistry, Manisa, Turkey. ece.onur@bayar.edu.tr
Background:
Behçet's disease (BD) is an inflammatory vasculitis. Endogenous nitric oxide (NO), produced by endothelial cells, has pleiotropic effects such as vasodilatator, antiplatelet, antiproliferative. Reactive oxygen species (ROS) are produced at sites of endothelial inflammation. ROS target polyunsaturated lipids, which results in malondialdehyde (MDA) production.
Objective:
The aim was to investigate the oxidative stress in BD patients by measuring MDA and total antioxidant status (TAS) levels and to establish a possible relationship with respect to NO levels regarding disease activity.
Materials And Methods:
55 BD patients (30 active/25 inactive) and 20 healthy volunteers were included in the study. Blood samples were drawn following an overnight fasting. TAS and MDA levels were determined spectrophotometrically. Serum nitrite (NO(2-)) and nitrate (NO(3-)) levels were measured to estimate NO production. Data were expressed as mean ± SD.
Results:
TAS levels were significantly lower in BD patients than the controls (1.19 ± 0.34 vs. 3.29 ± 0.89 mmol/L). In the active BD group, MDA levels (0.36 ± 0.19 nmol/mL) were significantly higher than both the inactive BD group (0.25 ± 0.18 nmol/mL) and controls (0.18 ± 0.41 nmol/mL). NO levels were significantly lower in the active group compared to the inactive group (18.0 ± 2.80 vs. 19.40 ± 2.70 µmol/L). MDA levels correlated negatively with NO levels in the active group.
Conclusion:
Decreased NO levels mediated by increased oxidative stress significantly contribute to endothelial dysfunction observed in BD.
Related Concept Videos
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
Coronary Artery Disease II: Pathophysiology
Coronary Artery Disease I: Introduction
Nitric Oxide Signaling Pathway

