scholarly journals Soluble guanylate cyclase redox state under oxidative stress conditions in isolated monkey coronary arteries

2016 ◽  
Vol 4 (5) ◽  
Author(s):  
Masashi Tawa ◽  
Tomio Okamura
Keyword(s):  
Oxidative Stress ◽  
Coronary Arteries ◽  
Guanylate Cyclase ◽  
Redox State ◽  
Soluble Guanylate Cyclase ◽  
Stress Conditions

Soluble Guanylate Cyclase Redox State Under Hypoxia or Hypoxia/Reoxygenation in Isolated Monkey Coronary Arteries

2014 ◽  
Vol 125 (2) ◽  
pp. 169-175 ◽  
Author(s):  
Masashi Tawa ◽  
Ayman Geddawy ◽  
Takashi Shimosato ◽  
Hirotaka Iwasaki ◽  
Takeshi Imamura ◽  
...  
Keyword(s):  
Coronary Arteries ◽  
Guanylate Cyclase ◽  
Redox State ◽  
Soluble Guanylate Cyclase ◽  
Hypoxia Reoxygenation

A manganese oxide nanozyme prevents the oxidative damage of biomolecules without affecting the endogenous antioxidant system

Nanoscale ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 3855-3863 ◽  
Author(s):  
Namrata Singh ◽  
Mohammed Azharuddin Savanur ◽  
Shubhi Srivastava ◽  
Patrick D'Silva ◽  
Govindasamy Mugesh
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Manganese Oxide ◽  
Antioxidant System ◽  
Mammalian Cells ◽  
Redox State ◽  
Stress Conditions ◽  
System P ◽  
Endogenous Antioxidant ◽  
Antioxidant Machinery

Multi-enzyme mimetic Mn3O4 nanoflowers (Mp) modulate the redox state of mammalian cells without altering the cellular antioxidant machinery under oxidative stress conditions.

Oxygen-elicited responses in calf coronary arteries: role of H2O2 production via NADH-derived superoxide

1996 ◽  
Vol 270 (3) ◽  
pp. H1044-H1053 ◽  
Author(s):  
K. M. Mohazzab-H ◽  
P. M. Kaminski ◽  
R. P. Fayngersh ◽  
M. S. Wolin
Keyword(s):  
Coronary Arteries ◽  
Guanylate Cyclase ◽  
Oxidase Activity ◽  
Soluble Guanylate Cyclase ◽  
Nadh Oxidase ◽  
Pulmonary Arteries ◽  
H2o2 Production ◽  
Oxidation Of Methanol ◽  
Nadh Oxidase Activity ◽  
Stimulation Of

Our previous studies in isolated endothelium-removed calf pulmonary arteries suggest that PO2-elicited responses are primarily mediated through modulation of guanosine 3',5'-cyclic monophosphate via changes in the generation of H2O2 originating from superoxide anion (O2-.) produced by NADH oxidase activity. In the present study we examined the importance of this mechanism in PO2-elicited responses of endothelium-removed calf coronary arteries. NADH oxidase activity was found to be the major source of O2-. in the homogenate of endothelium-removed calf coronary arteries detected by lucigenin-elicited chemiluminescence. Precontracted endothelium-removed calf coronary arteries show a relaxation to hypoxia, and reoxygenation causes a transient additional relaxation before the recovery of normoxic levels of force. Under these conditions the detection of O2-. was decreased by hypoxia and a transient overproduction was observed during reoxygenation. The relaxation to reoxygenation, but not to hypoxia, was significantly inhibited by a scavenger of O2-. that prevents the formation of H2O2 (nitro blue tetrazolium), an inhibitor of NAD(P)H oxidases and other O2(-.)-generating flavoproteins (diphenyliodonium), and inhibition of the stimulation of soluble guanylate cyclase (LY-83583). A scavenger of O2-. that promotes H2O2 formation (Tiron) did not inhibit the PO2-elicited responses examined. Hypoxia and diphenyliodonium (but not Tiron) decreased the metabolism of endogenous H2O2 by catalase (as measured by the H2O2-dependent co-oxidation of methanol to formaldehyde by catalase), and reoxygenation caused a stimulation of H2O2 metabolism by catalase. The presence of endothelium resulted in minor modifications of the PO2 responses, which were partially mediated via prostaglandins and nitric oxide on the basis of the effects of indomethacin and nitro-L-arginine, respectively. These results suggest that in calf coronary arteries the stimulation of guanylate cyclase via H2O2 originating from NADH-derived O2-(.) production contributes to the transient relaxation to posthypoxic reoxygenation, but not the response to hypoxia.

scholarly journals Therapeutic potential of soluble guanylate cyclase modulators in neonatal chronic lung disease

2015 ◽  
Vol 309 (10) ◽  
pp. L1037-L1040 ◽  
Author(s):  
Gerry T. M. Wagenaar ◽  
Pieter S. Hiemstra ◽  
Reinoud Gosens
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Hypertension ◽  
Lung Injury ◽  
Guanylate Cyclase ◽  
Premature Birth ◽  
Soluble Guanylate Cyclase ◽  
Therapeutic Potential ◽  
Vascular Development ◽  
Supplemental Oxygen ◽  
Neonatal Lung

Supplemental oxygen after premature birth results in aberrant airway, alveolar, and pulmonary vascular development with an increased risk for bronchopulmonary dysplasia, and development of wheeze and asthma, pulmonary hypertension, and chronic obstructive pulmonary disease in survivors. Although stimulation of the nitric oxide (NO)-soluble guanylate cyclase (sGC)-cGMP signal transduction pathway has significant beneficial effects on disease development in animal models, so far this could not be translated to the clinic. Oxidative stress reduces the NO-sGC-cGMP pathway by oxidizing heme-bound sGC, resulting in inactivation or degradation of sGC. Reduced sGC activity and/or expression is associated with pathology due to premature birth, oxidative stress-induced lung injury, including impaired alveolar maturation, smooth muscle cell (SMC) proliferation and contraction, impaired airway relaxation and vasodilation, inflammation, pulmonary hypertension, right ventricular hypertrophy, and an aggravated response toward hyperoxia-induced neonatal lung injury. Recently, Britt et al. (10) demonstrated that histamine-induced Ca2+ responses were significantly elevated in hyperoxia-exposed fetal human airway SMCs compared with normoxic controls and that this hyperoxia-induced increase in the response was strongly reduced by NO-independent stimulation and activation of sGC. These recent studies highlight the therapeutic potential of sGC modulators in the treatment of preterm infants for respiratory distress with supplemental oxygen. Such treatment is aimed at improving aberrant alveolar and vascular development of the neonatal lung and preventing the development of wheezing and asthma in survivors of premature birth. In addition, these studies highlight the suitability of fetal human airway SMCs as a translational model for pathological airway changes in the neonate.

scholarly journals The uremic retention solute p-cresyl sulfate alters NO signal transduction by alteration of the soluble guanylate cyclase redox state

2009 ◽  
Vol 9 (S1) ◽  
Author(s):  
Björn KI Meijers ◽  
Constanze Meye ◽  
Johannes-Peter Stasch ◽  
Peter Gross ◽  
Pieter Evenepoel
Keyword(s):  
Signal Transduction ◽  
Guanylate Cyclase ◽  
Redox State ◽  
Soluble Guanylate Cyclase

scholarly journals Cytochrome b5 Reductase 3 Modulates Soluble Guanylate Cyclase Redox State and cGMP Signaling

2017 ◽  
Vol 121 (2) ◽  
pp. 137-148 ◽  
Author(s):  
Mizanur M. Rahaman ◽  
Anh T. Nguyen ◽  
Megan P. Miller ◽  
Scott A. Hahn ◽  
Courtney Sparacino-Watkins ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
Redox State ◽  
Soluble Guanylate Cyclase ◽  
Cytochrome B5 ◽  
Cytochrome B5 Reductase ◽  
Cgmp Signaling

scholarly journals Comparison of Soluble Guanylate Cyclase Stimulators and Activators in Models of Cardiovascular Disease Associated with Oxidative Stress

2012 ◽  
Vol 3 ◽  
Author(s):  
Melissa H. Costell ◽  
Nicolas Ancellin ◽  
Roberta E. Bernard ◽  
Shufang Zhao ◽  
John J. Upson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase

scholarly journals Alteration of the soluble guanylate cyclase system in coronary arteries of high cholesterol diet‐fed rabbits

2021 ◽  
Vol 9 (4) ◽  
Author(s):  
Masashi Tawa ◽  
Katsuya Nakano ◽  
Yuka Yamashita ◽  
Qiang He ◽  
Takayoshi Masuoka ◽  
...  
Keyword(s):  
Coronary Arteries ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol
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