Premium
Effects of NADPH oxidase inhibitor apocynin on real‐time blood hydrogen peroxide release in femoral artery/vein ischemia and reperfusion
Author(s) -
Parker C. Woodworth,
Bartol Kyle D,
Perkins Kerry-Anne,
Chen Qian,
Young Lindon H
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.678.8
Subject(s) - apocynin , nadph oxidase , femoral artery , femoral vein , oxidative stress , ischemia , hydrogen peroxide , chemistry , pharmacology , nitric oxide , medicine , blood vessel , oxidase test , anesthesia , endocrinology , biochemistry , enzyme
Vascular endothelial dysfunction can initiate oxidative stress during ischemia/reperfusion (I/R). Endothelial dysfunction is characterized by an increase in blood hydrogen peroxide (H 2 O 2 ) and a decrease in endothelial‐derived nitric oxide (NO) bioavailability. Previous studies using Gö 6983, a broad‐spectrum protein kinase C inhibitor that can inhibit NADPH oxidase activity, has attenuated blood H 2 O 2 levels during femoral I/R in vivo . This study examines the effects of apocynin, a direct NADPH oxidase inhibitor, on real‐time blood H 2 O 2 levels in femoral I/R in vivo . H 2 O 2 microsensors (100 μm) were inserted into both femoral veins in anesthetized rats. One hind limb was subjected to ischemia by clamping the femoral artery and vein for 20 minutes and allowed to reperfuse for 45 minutes, while the other hind limb served as a sham. In the control group, H 2 O 2 was significantly increased by 1.3–2.7 μM during 45 minutes of reperfusion in the I/R vein when compared to the sham vein (n=4, P<0.05). Intravenous apocynin (13.7 mg/kg) given at the beginning of reperfusion significantly decreased blood H 2 O 2 levels compared to the control group (n=6, P<0.05). The data suggests that apocynin attenuates oxidative stress in femoral I/R, which may be due to inhibition of leukocyte/endothelial NADPH oxidase.