scholarly journals Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis

2009 ◽  
Vol 297 (2) ◽  
pp. L209-L216 ◽  
Author(s):  
Gin C. Chuang ◽  
Zhen Yang ◽  
David G. Westbrook ◽  
Melissa Pompilius ◽  
Carol A. Ballinger ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Molecular Mechanisms ◽  
Hospital Admissions ◽  
Vascular Dysfunction ◽  
Oxidant Stress ◽  
Atherosclerotic Lesion ◽  
The United States ◽  
Mitochondrial Damage ◽  
Ozone Exposure ◽  
Environmental Toxicants

More than 100 million people in the United States live in areas that exceed current ozone air quality standards. In addition to its known pulmonary effects, environmental ozone exposures have been associated with increased hospital admissions related to cardiovascular events, but to date, no studies have elucidated the potential molecular mechanisms that may account for exposure-related vascular impacts. Because of the known pulmonary redox and immune biology stemming from ozone exposure, we hypothesized that ozone inhalation would initiate oxidant stress, mitochondrial damage, and dysfunction within the vasculature. Accordingly, these factors were quantified in mice consequent to a cyclic, intermittent pattern of ozone or filtered air control exposure. Ozone significantly modulated vascular tone regulation and increased oxidant stress and mitochondrial DNA damage (mtDNA), which was accompanied by significantly decreased vascular endothelial nitric oxide synthase protein and indices of nitric oxide production. To examine influences on atherosclerotic lesion formation, apoE−/− mice were exposed as above, and aortic plaques were quantified. Exposure resulted in significantly increased atherogenesis compared with filtered air controls. Vascular mitochondrial damage was additionally quantified in ozone- and filtered air-exposed infant macaque monkeys. These studies revealed that ozone increased vascular mtDNA damage in nonhuman primates in a fashion consistent with known atherosclerotic lesion susceptibility in humans. Consequently, inhaled ozone, in the absence of other environmental toxicants, promotes increased vascular dysfunction, oxidative stress, mitochondrial damage, and atherogenesis.

scholarly journals Nitric Oxide, Oxidative Stress, andp66ShcInterplay in Diabetic Endothelial Dysfunction

2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Alessandra Magenta ◽  
Simona Greco ◽  
Maurizio C. Capogrossi ◽  
Carlo Gaetano ◽  
Fabio Martelli
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Diabetic Patients ◽  
Oxygen Species ◽  
Complex Interplay ◽  
Cell Dysfunction ◽  
Intracellular Ros ◽  
No Bioavailability

Increased oxidative stress and reduced nitric oxide (NO) bioavailability play a causal role in endothelial cell dysfunction occurring in the vasculature of diabetic patients. In this review, we summarized the molecular mechanisms underpinning diabetic endothelial and vascular dysfunction. In particular, we focused our attention on the complex interplay existing among NO, reactive oxygen species (ROS), and one crucial regulator of intracellular ROS production,p66Shcprotein.

scholarly journals The human uterine smooth muscle S-nitrosoproteome fingerprint in pregnancy, labor, and preterm labor

2013 ◽  
Vol 305 (8) ◽  
pp. C803-C816 ◽  
Author(s):  
Craig Ulrich ◽  
David R. Quilici ◽  
Karen A. Schlauch ◽  
Iain L. O. Buxton
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Preterm Delivery ◽  
Preterm Labor ◽  
Molecular Mechanisms ◽  
Area Under The Curve ◽  
Soluble Guanylyl Cyclase ◽  
The United States ◽  
Nitric Oxide Donor ◽  
Uterine Smooth Muscle

Molecular mechanisms involved in uterine quiescence during gestation and those responsible for induction of labor at term are incompletely known. More than 10% of babies born worldwide are premature and 1,000,000 die annually. Preterm labor results in preterm delivery in 50% of cases in the United States explaining 75% of fetal morbidity and mortality. There is no Food and Drug Administration-approved treatment to prevent preterm delivery. Nitric oxide-mediated relaxation of human uterine smooth muscle is independent of global elevation of cGMP following activation of soluble guanylyl cyclase. S-nitrosation is a likely mechanism to explain cGMP-independent relaxation to nitric oxide and may reveal S-nitrosated proteins as new therapeutic targets for the treatment of preterm labor. Employing S-nitrosoglutathione as an nitric oxide donor, we identified 110 proteins that are S-nitrosated in 1 or more states of human pregnancy. Using area under the curve of extracted ion chromatograms as well as normalized spectral counts to quantify relative expression levels for 62 of these proteins, we show that 26 proteins demonstrate statistically significant S-nitrosation differences in myometrium from spontaneously laboring preterm patients compared with nonlaboring patients. We identified proteins that were up- S-nitrosated as well as proteins that were down- S-nitrosated in preterm laboring tissues. Identification and relative quantification of the S-nitrosoproteome provide a fingerprint of proteins that can form the basis of hypothesis-directed efforts to understand the regulation of uterine contraction-relaxation and the development of new treatment for preterm labor.

scholarly journals Healthberry 865® and Its Related, Specific, Single Anthocyanins Exert a Direct Vascular Action, Modulating Both Endothelial Function and Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1191
Author(s):  
Albino Carrizzo ◽  
Rosario Lizio ◽  
Paola Di Pietro ◽  
Michele Ciccarelli ◽  
Antonio Damato ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nadph Oxidase ◽  
Intracellular Signaling ◽  
Vascular Reactivity ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Epidemiological Studies ◽  
Direct Role ◽  
And Oxidative Stress

In recent years, epidemiological studies have identified a relationship between diet and cerebro–cardiovascular disease (CVD). In this regard, there is a promising dietary group for cardiovascular protection are polyphenols, especially anthocyanins. Vascular reactivity studies were performed using Healthberry 865® and constituent single anthocyanins to characterize vasomotor responses; immunofluorescence analysis with dichlorofluorescein diacetate and dihydroethidium were used to evaluate nitric oxide and oxidative stress; lucigenin assay was used to measure NADPH oxidase activity; and gel electrophoresis and immunoblotting were used to dissect the molecular mechanisms involved. We demonstrated that Healthberry 865® exerts an important vasorelaxant effect of resistance artery functions in mice. Its action is mediated by nitric oxide release through the intracellular signaling PI3K/Akt. Moreover, behind its capability of modulating vascular tone, it also exerts an important antioxidant effect though the modulation of the NADPH oxidase enzyme. Interestingly, its cardiovascular properties are mediated by the selective action of different anthocyanins. Finally, the exposure of human dysfunctional vessels to Healthberry 865® significantly reduces oxidative stress and improves NO bioavailability. Although further investigations are needed, our data demonstrate the direct role of Healthberry 865® on the modulation of vasculature, both on the vasorelaxation and on oxidative stress; thus, supporting the concept that a pure mixture of anthocyanins could be helpful in preventing the onset of vascular dysfunction associated with the development of CVD.

scholarly journals Modulation of Fibrosis in Systemic Sclerosis by Nitric Oxide and Antioxidants

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Audrey Dooley ◽  
K. Richard Bruckdorfer ◽  
David J. Abraham
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Systemic Sclerosis ◽  
Free Radical ◽  
Animal Models ◽  
Connective Tissue ◽  
Vascular Dysfunction ◽  
Oxidant Stress ◽  
Unknown Aetiology ◽  
Protective System

Systemic sclerosis (scleroderma: SSc) is a multisystem, connective tissue disease of unknown aetiology characterized by vascular dysfunction, autoimmunity, and enhanced fibroblast activity resulting in fibrosis of the skin, heart, and lungs, and ultimately internal organ failure, and death. One of the most important and early modulators of disease activity is thought to be oxidative stress. Evidence suggests that the free radical nitric oxide (NO), a key mediator of oxidative stress, can profoundly influence the early microvasculopathy, and possibly the ensuing fibrogenic response. Animal models and human studies have also identified dietary antioxidants, such as epigallocatechin-3-gallate (EGCG), to function as a protective system against oxidative stress and fibrosis. Hence, targeting EGCG may prove a possible candidate for therapeutic treatment aimed at reducing both oxidant stress and the fibrotic effects associated with SSc.

Cost-Effectiveness of Inhaled Nitric Oxide in the Treatment of Neonatal Respiratory Failure in the United States

PEDIATRICS ◽  
2003 ◽  
Vol 112 (6) ◽  
pp. 1351-1360 ◽  
Author(s):  
D. C. Angus ◽  
G. Clermont ◽  
R. S. Watson ◽  
W. T. Linde-Zwirble ◽  
R. H. Clark ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
United States ◽  
Cost Effectiveness ◽  
Respiratory Failure ◽  
The United States ◽  
Inhaled Nitric Oxide

Aminoguanidine, a novel inhibitor of nitric oxide formation, prevents diabetic vascular dysfunction

Diabetes ◽  
1992 ◽  
Vol 41 (4) ◽  
pp. 552-556 ◽  
Author(s):  
J. A. Corbett ◽  
R. G. Tilton ◽  
K. Chang ◽  
K. S. Hasan ◽  
Y. Ido ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Oxide Formation ◽  
Nitric Oxide Formation

The Signaling Pathways in Nitric Oxide Production by Neutrophils Exposed to N-nitrosodimethylamine

2018 ◽  
Vol 16 (2) ◽  
pp. 194-199
Author(s):  
Wioletta Ratajczak-Wrona ◽  
Ewa Jablonska
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Polymorphonuclear Neutrophils ◽  
Microbial Pathogens ◽  
Human Neutrophils ◽  
No Production ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Background: Polymorphonuclear neutrophils (PMNs) play a crucial role in the innate immune system’s response to microbial pathogens through the release of reactive nitrogen species, including Nitric Oxide (NO). </P><P> Methods: In neutrophils, NO is produced by the inducible Nitric Oxide Synthase (iNOS), which is regulated by various signaling pathways and transcription factors. N-nitrosodimethylamine (NDMA), a potential human carcinogen, affects immune cells. NDMA plays a major part in the growing incidence of cancers. Thanks to the increasing knowledge on the toxicological role of NDMA, the environmental factors that condition the exposure to this compound, especially its precursors- nitrates arouse wide concern. Results: In this article, we present a detailed summary of the molecular mechanisms of NDMA’s effect on the iNOS-dependent NO production in human neutrophils. Conclusion: This research contributes to a more complete understanding of the mechanisms that explain the changes that occur during nonspecific cellular responses to NDMA toxicity.

Diabetes Discharge Planning and Transitions of Care: A Focused Review

2019 ◽  
Vol 15 (2) ◽  
pp. 111-117 ◽  
Author(s):  
Robin L. Black ◽  
Courtney Duval
Keyword(s):  
Patient Outcomes ◽  
Hospital Admissions ◽  
Discharge Planning ◽  
Medication Management ◽  
Hospital Readmissions ◽  
The United States ◽  
Transitions Of Care ◽  
Discharge Process ◽  
The Impact ◽  
Diabetes Patients

Background: Diabetes is a growing problem in the United States. Increasing hospital admissions for diabetes patients demonstrate the need for evidence-based care of diabetes patients by inpatient providers, as well as the importance of continuity of care when transitioning patients from inpatient to outpatient providers. Methods: A focused literature review of discharge planning and transitions of care in diabetes, conducted in PubMed is presented. Studies were selected for inclusion based on content focusing on transitions of care in diabetes, risk factors for readmission, the impact of inpatient diabetes education on patient outcomes, and optimal medication management of diabetes during care transitions. American Diabetes Association (ADA) guidelines for care of patients during the discharge process are presented, as well as considerations for designing treatment regimens for a hospitalized patient transitioning to various care settings. Results: Multiple factors may make transitions of care difficult, including poor communication, poor patient education, inappropriate follow-up, and clinically complex patients. ADA recommendations provide guidance, but an individualized approach for medication management is needed. Use of scoring systems may help identify patients at higher risk for readmission. Good communication with patients and outpatient providers is needed to prevent patient harm. A team-based approach is needed, utilizing the skills of inpatient and outpatient providers, diabetes educators, nurses, and pharmacists. Conclusion: Structured discharge planning per guideline recommendations can help improve transitions in care for patients with diabetes. A team based, patient-centered approach can help improve patient outcomes by reducing medication errors, delay of care, and hospital readmissions.

Molecular Mechanisms of Curcumin in Neuroinflammatory Disorders: A Mini Review of Current Evidences

2019 ◽  
Vol 19 (3) ◽  
pp. 247-258 ◽  
Author(s):  
Mahsa Hatami ◽  
Mina Abdolahi ◽  
Neda Soveyd ◽  
Mahmoud Djalali ◽  
Mansoureh Togha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
English Language ◽  
Molecular Mechanisms ◽  
Randomized Clinical Trials ◽  
Mitochondrial Dynamics ◽  
Nuclear Factor Κb ◽  
General Term ◽  
Neuroinflammatory Disease ◽  
Tnf Α ◽  
Factor Α

Objective: Neuroinflammatory disease is a general term used to denote the progressive loss of neuronal function or structure. Many neuroinflammatory diseases, including Alzheimer’s, Parkinson’s, and multiple sclerosis (MS), occur due to neuroinflammation. Neuroinflammation increases nuclear factor-κB (NF-κB) levels, cyclooxygenase-2 enzymes and inducible nitric oxide synthase, resulting in the release of inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). It could also lead to cellular deterioration and symptoms of neuroinflammatory diseases. Recent studies have suggested that curcumin (the active ingredient in turmeric) could alleviate the process of neuroinflammatory disease. Thus, the present mini-review was conducted to summarize studies regarding cellular and molecular targets of curcumin relevant to neuroinflammatory disorders. Methods: A literature search strategy was conducted for all English-language literature. Studies that assessed the various properties of curcuminoids in respect of neuroinflammatory disorders were included in this review. Results: The studies have suggested that curcuminoids have significant anti- neuroinflammatory, antioxidant and neuroprotective properties that could attenuate the development and symptom of neuroinflammatory disorders. Curcumin can alleviate neurodegeneration and neuroinflammation through multiple mechanisms, by reducing inflammatory mediators (such as TNF-α, IL-1β, nitric oxide and NF-κB gene expression), and affect mitochondrial dynamics and even epigenetic changes. Conclusion: It is a promising subject of study in the prevention and management of the neuroinflammatory disease. However, controlled, randomized clinical trials are needed to fully evaluate its clinical potential.

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