Nitric oxide donor prevents hydrogen peroxide-mediated endothelial cell injury

Chang, Jong San; Rao, Narayanam V.; Markewitz, Boaz A.; Hoidal, John R.; Michael, John R.

doi:10.1152/ajplung.1996.270.6.l931

Cited by 45 publications

(50 citation statements)

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“…These functions include modulation of vasoactivity and blood pressure, and inhibition of platelet aggregation, leukocyte adhesion and smooth muscle cell proliferation (Limbourg et al, 2002;Jugdutt, 2002;Papapetropoulos et al, 1999). Additionally, several studies have demonstrated that NO acts as an antioxidant (Chang et al, 1996;Hermann et These autocrine and paracrine actions of NO ultimately facilitate vascular differentiation and development. In the hyperglycemic condition, endodermal iNOS expression is maintained and the resultant increased NO generated participates with SO to generate increased ROS levels, which, in turn, affect the numerous soluble factors required for mesodermal differentiation and migration.…”

Section: Discussionmentioning

confidence: 99%

“…Studies using low doses of NO donors demonstrated that NO directly acts as an antioxidant (Chang et al, 1996;Joshi et al, 1999;Kim et al, 1995;Wink et al, 1993). Therefore, we hypothesized that the vasculopathy induced by L-NMMA may be due to increased ROS, suggesting a common pathway with hyperglycemia.…”

Section: No Depletion Increases Ros Production: a Common Pathway In Vmentioning

confidence: 96%

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Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

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Nitric oxide (NO) has been demonstrated to mediate events during ovulation,pregnancy, blastocyst invasion and preimplantation embryogenesis. However,less is known about the role of NO during postimplantation development. Therefore, in this study, we explored the effects of NO during vascular development of the murine yolk sac, which begins shortly after implantation. Establishment of the vitelline circulation is crucial for normal embryonic growth and development. Moreover, functional inactivation of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during this period leads to embryonic defects/lethality, as this structure is vital for transport, metabolism and induction of vascular development. In this study, we describe the temporally/spatially regulated distribution of nitric oxide synthase (NOS) isoforms during the three stages of yolk sac vascular development (blood island formation, primary capillary plexus formation and vessel maturation/remodeling) and found NOS expression patterns were diametrically opposed. To pharmacologically manipulate vascular development,an established in vitro system of whole murine embryo culture was employed. During blood island formation, the endoderm produced NO and inhibition of NO(L-NMMA) at this stage resulted in developmental arrest at the primary plexus stage and vasculopathy. Furthermore, administration of a NO donor did not cause abnormal vascular development; however, exogenous NO correlated with increased eNOS and decreased iNOS protein levels. Additionally, a known environmental insult (high glucose) that produces reactive oxygen species(ROS) and induces vasculopathy also altered eNOS/iNOS distribution and induced NO production during yolk sac vascular development. However, administration of a NO donor rescued the high glucose induced vasculopathy, restored the eNOS/iNOS distribution and decreased ROS production. These data suggest that NO acts as an endoderm-derived factor that modulates normal yolk sac vascular development, and decreased NO bioavailability and NO-mediated sequela may underlie high glucose induced vasculopathy.

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Section: Discussionmentioning

confidence: 99%

Section: No Depletion Increases Ros Production: a Common Pathway In Vmentioning

confidence: 96%

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

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“…37) The mechanism of the protected effect may be explained by high affinity binding of NO 37,38) since NO can react with O 2 −· to generate peroxynitrite radicals. AFIM has been previously shown to confer improved resistance against ischemic/reperfused injury 39) ; we wished to verify that it could also protect the antioxidase activity in hypobaric hypoxia mice.…”

Section: )mentioning

confidence: 99%

Anti-hypoxia Activity of the Novel NO Donor Acetyl Ferulic Isosorbide Mononitrate in Acute High-Altitude Hypoxia Mice

Fan

Jiang

et al. 2015

Biological & Pharmaceutical Bulletin

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Nitric oxide (NO) may act as either a pro-oxidant or an antioxidant in biological systems. Previous work has found inhalation of NO improved survival in a high altitude rat model. NO donor isosorbide mononitrate derivants might have a protective effect against hypoxia. We synthesized a series of isosorbide mononitrate derivant compounds to test their anti-hypoxia activities. Normobaric hypoxia and hypobaric hypoxia models were used to study the protective role of NO donor in mice. The results showed isosorbide mononitrate derivants had protective effects in hypoxia mice. Among those compounds, acetyl ferulic isosorbide mononitrate (AFIM) was the most effective. It prolonged the survival time during the normobaric hypoxia test. It decreased malondialdehyde (MDA) and H 2 O 2 in hypobaric hypoxia mice. The antioxidase activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) remained in normal ranges in the AFIM group. As a sign of mitochondrial dysfunction, the activities of ATPase were down regulated in mice under hypobaric hypoxia conditions. AFIM also protected ATPase activities. The protective effects of AFIM might come from a sustained NO supply and the release of acetyl ferulic acid with anti-oxidant activity.Key words altitude; hypoxia; nitric oxide; acetyl ferulic isosorbide mononitrate More than 140 M persons lives at above 2500 m (the conventional definition of high altitude as that where arterial O 2 saturation (SaO 2 ) measurably begins to fall).1) Barometric pressure falls with increasing altitude and consequently there is a reduction in the partial pressure of oxygen resulting in a hypoxic challenge to any individual ascending to altitude. With the ever increasing number of people ascending to high altitudes, medicines to deal with potential problems are becoming increasingly relevant to non-specialists, including general practitioners.A spectrum of high altitude illnesses can occur when the hypoxic stress outstrips the subject's ability to acclimatize. Acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) strike people who travel too fast to high altitudes that lie beyond their current level of acclimatization. 2)AMS is a condition affecting otherwise healthy individuals on going rapidly to altitude. A spectrum of symptoms related to acute mountain sickness may develop at altitudes below 3000 m: commonly reported symptoms are nausea, vomiting, headache, dizziness, fatigue, and sleep disturbance. 3)Acute hypoxia induces pulmonary vascular permeability and contributes to forms of noncardiogenic pulmonary edema such as high altitude pulmonary edema and acute respiratory distress syndrome.4,5) AMS can sharply limit recreation and work at high altitude, especially in the first few days following arrival at a new, higher altitude, and if AMS worsens and HACE develops, the risk of fatality is significant. 6) Although slow ascent to altitude remained the most important measure to prevent acute mountain sickness, evidence from the literature on high altitude...

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“…In another set of experiments, different concentrations of exogenous bilirubin were applied to cells for 2 h. At the end of the incubation, cells were washed and exposed for 2 h to fresh culture medium containing various concentrations (10-120 m-units\ml) of glucose oxidase (GOX), an enzyme that catalyses the conversion of -glucose to -gluconolactone, producing hydrogen peroxide at constant rate. This oxidant-generating system has been used previously in cell culture in itro to promote oxidative injury [21]. Cell viability was assessed using a colorimetric assay kit from Promega (Madison, WI, U.S.A.) according to manufacturers' instructions.…”

Section: Cytotoxicity Assaymentioning

confidence: 99%

Dynamics of haem oxygenase-1 expression and bilirubin production in cellular protection against oxidative stress

Clark

Foresti

Green

et al. 2000

Biochemical Journal

217

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The inducible isoform of haem oxygenase (HO-1) has been proposed as an effective system to counteract oxidant-induced cell injury. In several circumstances, this cytoprotective effect has been attributed to increased generation of the antioxidant bilirubin during haem degradation by HO-1. However, a direct implication for HO-1-derived bilirubin in protection against oxidative stress remains to be established. In the present study, we examined the dynamics of HO-1 expression and bilirubin production after stimulation of vascular smooth-muscle cells with hemin, a potent inducer of the HO-1 gene. We found that hemin-mediated increase in HO-1 protein expression and haem oxygenase activity is associated with augmented bilirubin levels. The majority of bilirubin production occurred early after exposure of cells to hemin. Hemin pre-treatment also resulted in high resistance to cell injury caused by an oxidant-generating system. Interestingly, this protective effect was manifest only when cells were actively producing bilirubin as a consequence of increased haem availability and utilization by HO-1. Tin protoporphyrin IX, an inhibitor of haem oxygenase activity, significantly reduced bilirubin generation and reversed cellular protection afforded by hemin treatment. Furthermore, addition of bilirubin to the culture medium markedly reduced the cytotoxicity produced by oxidants. Our findings provide direct evidence that bilirubin generated after up-regulation of the HO-1 pathway is cytoprotective against oxidative stress.

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Nitric oxide donor prevents hydrogen peroxide-mediated endothelial cell injury

Cited by 45 publications

References 0 publications

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

Anti-hypoxia Activity of the Novel NO Donor Acetyl Ferulic Isosorbide Mononitrate in Acute High-Altitude Hypoxia Mice

Dynamics of haem oxygenase-1 expression and bilirubin production in cellular protection against oxidative stress

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