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Reactive oxygen species metabolism in veins and arteries from rat: why is it different?
Author(s) -
Szasz Irina Theodora,
Rondelli Catherine M,
Fink Gregory D,
Watts Stephanie W
Publication year - 2006
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.20.4.a725-c
Subject(s) - oxidative stress , xanthine oxidase , reactive oxygen species , superoxide dismutase , catalase , superoxide , chemistry , medicine , mesenteric arteries , biochemistry , endocrinology , biology , artery , enzyme
Oxidative stress plays an important pathophysiological role in the development of cardiovascular diseases. The imbalance of pro and antioxidant factors, defining oxidative stress, occurs when production of reactive oxygen species (ROS) by generators (NADPH oxidase, xanthine oxidase, uncoupled NO synthase, lipoxygenases, cyclooxygenases or the mitochondrial electron transport chain) overcomes cellular protection provided by defense systems (superoxide dismutase, catalase, glutathione and nonenzymatic scavengers). Our laboratory is researching the role of veins in the development of hypertension. We investigated ROS generation and some of its major determinants in venous and arterial blood vessels from normal rats. The superior mesenteric vein (SMV) and artery (SMA), as well as the inferior vena cava (VC) and the thoracic aorta (Ao) were compared in terms of their basal superoxide production relative to tissue weight, using a lucigenin chemiluminiscence based assay. In both cases, the vein generated more superoxide than its arterial counterpart (VC = 210 ± 42% Ao; SMV = 267 ± 48% SMA). Western analysis of homogenates from rat VC and Ao revealed that xanthine oxidase expression was significantly increased in the VC compared to the Ao (280 ± 31%), as well as catalase expression (VC = 135 ± 11% Ao) while p47 phox had decreased expression in the VC compared to Ao (70 ± 11%). No significant change was observed for eNOS, RAC1 and Cu Zn SOD. These data suggest that veins differ from arteries with respect to ROS metabolism. However, the molecular mechanisms behind the different ROS handling by venous and arterial vascular tissue have yet to be uncovered.