Effects of 1-MCP on reactive oxygen species, polyphenol oxidase activity, and cellular ultra-structure of core tissue in ‘Yali’ pear (Pyrus bretschneideri Rehd.) during Storage

Recent studies have suggested that oxidative stress may be involved in the development of arterial aneurysms. Xanthine oxidase is implicated in the generation of reactive oxygen species under pathological conditions in the cardiovascular system, and increased xanthine oxidase activity has been reported in human aortic aneurysms. We, therefore, studied the changes of xanthine oxidase activity and oxidative stress in human ruptured cerebral aneurysms. Six cerebral aneurysmal samples were obtained during surgery. Normal arteries of the similar size (one superficial temporal artery, four uterine arteries and three right gastroepiploic arteries) were used as controls. The xanthine oxidase activity was measured with a commercial assay kit, and its expression was localized by immunohistochemistry. The xanthine oxidase activity was significantly increased in aneurysms by 4.1 fold (P<0.05) compared to control arteries. This was accompanied by an elevated malondialdehyde (MDA) level (8.3±5.1 versus 2.9±0.7 nmol/g protein, mean ±SD, P<0.05), a marker of oxidative stress. Immunohistochemistry established that xanthine oxidase was mainly expressed in infiltrating inflammatory cells. Our study indicates that xanthine oxidase may have an important role in the increased oxidative stress in ruptured cerebral aneurysms. Further studies are needed to clarify the role of XO-derived reactive oxygen species in the development and rupture of cerebral aneurysms.

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D5 dopamine receptor regulation of reactive oxygen species production, NADPH oxidase, and blood pressure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00434.2005 ◽

2006 ◽

Vol 290 (1) ◽

pp. R96-R104 ◽

Cited By ~ 79

Author(s):

Zhiwei Yang ◽

Laureano D. Asico ◽

Peiying Yu ◽

Zheng Wang ◽

John E. Jones ◽

...

Keyword(s):

Blood Pressure ◽

Reactive Oxygen Species ◽

Nadph Oxidase ◽

Oxidase Activity ◽

Reactive Oxygen ◽

Receptor Activation ◽

Oxidase Inhibitor ◽

Ros Production ◽

Oxygen Species ◽

Nadph Oxidase Activity

Activation of D1-like receptors (D1 and/or D5) induces antioxidant responses; however, the mechanism(s) involved in their antioxidant actions are not known. We hypothesized that stimulation of the D5 receptor inhibits NADPH oxidase activity, and thus the production of reactive oxygen species (ROS). We investigated this issue in D5 receptor-deficient (D5−/−) and wild-type (D5+/+) mice. NADPH oxidase protein expression (gp91phox, p47phox, and Nox 4) and activity in kidney and brain, as well as plasma thiobarbituric acid-reactive substances (TBARS) were higher in D5−/− than in D5+/+ mice. Furthermore, apocynin, an NADPH oxidase inhibitor, normalized blood pressure, renal NADPH oxidase activity, and plasma TBARS in D5−/− mice. In HEK-293 cells that heterologously expressed human D5 receptor, its agonist fenoldopam decreased NADPH oxidase activity, expression of one of its subunits (gp91phox), and ROS production. The inhibitory effect of the D5 receptor activation on NADPH oxidase activity was independent of cAMP/PKA but was partially dependent on phospholipase D2. The ability of D5 receptor stimulation to decrease ROS production may explain, in part, the antihypertensive action of D5 receptor activation.

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Comparative effects of pitavastatin and probucol on oxidative stress, Cu/Zn superoxide dismutase, PPAR-γ, and aortic stiffness in hypercholesterolemia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01198.2005 ◽

2006 ◽

Vol 291 (5) ◽

pp. H2522-H2532 ◽

Cited By ~ 53

Author(s):

Kyoko Umeji ◽

Seiji Umemoto ◽

Shinichi Itoh ◽

Masakazu Tanaka ◽

Shinji Kawahara ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Superoxide Dismutase ◽

Oxidase Activity ◽

Aortic Stiffness ◽

Reactive Oxygen ◽

Oxygen Species ◽

Ppar Γ ◽

Expression And Activity

Reactive oxygen species-scavenging enzyme Cu/Zn superoxide dismutase (SOD) regulated by peroxisome proliferator-activated receptors (PPARs) plays an important role in vascular responsiveness. However, it remains unknown whether statin restores vascular dysfunction through the activation of reactive oxygen species-scavenging enzymes in vivo. We hypothesized that pitavastatin restores vascular function by modulating oxidative stress through the activation of Cu/ZnSOD and PPAR-γ in hypercholesterolemia. New Zealand White male rabbits were fed either normal chow or a 1% cholesterol (CHO) diet for 14 wk. After the first 7 wk, the CHO-fed rabbits were further divided into three groups: those fed with CHO feed only (HC), those additionally given pitavastatin, and those additionally given an antioxidant, probucol. The extent of atherosclerosis was assessed by examining aortic stiffness. When compared with the HC group, both the pitavastatin and probucol groups showed improved aortic stiffness by reducing aortic levels of reactive oxidative stress, nitrotyrosine, and collagen, without affecting serum cholesterol or blood pressure levels. Pitavastatin restored both Cu/ZnSOD activity ( P < 0.005) and PPAR-γ expression and activity ( P < 0.01) and inhibited NAD(P)H oxidase activity ( P < 0.0001) in the aorta, whereas probucol inhibited NAD(P)H oxidase activity more than did pitavastatin ( P < 0.0005) without affecting Cu/ZnSOD activity or PPAR-γ expression and activity. Importantly, Cu/ZnSOD activity was positively correlated with the PPAR-γ activity in the aorta ( P < 0.005), both of which were negatively correlated with aortic stiffness ( P < 0.05). Vascular Cu/ZnSOD and PPAR-γ may play a crucial role in the antiatherogenic effects of pitavastatin in hypercholesterolemia in vivo.

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