vanadium/inflamação

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Inflammatory cytokine release from human peripheral blood mononuclear cells exposed to polyetheretherketone and titanium-6 aluminum-4 vanadium in vitro.

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Objective To investigate the cytokine expression profiles of blood cells exposed to polyetheretherketone and titanium-6 aluminum-4 vanadium materials in vitro. Materials and methods Coin-shaped samples composed of titanium-6 aluminum-4 vanadium, polyetheretherketone, and blasted polyetheretherketone

Role of Vanadium in Cellular and Molecular Immunology: Association with Immune-Related Inflammation and Pharmacotoxicology Mechanisms.

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Over the last decade, a diverse spectrum of vanadium compounds has arisen as anti-inflammatory therapeutic metallodrugs targeting various diseases. Recent studies have demonstrated that select well-defined vanadium species are involved in many immune-driven molecular mechanisms that regulate and

Vanadium-induced chemokine mRNA expression and pulmonary inflammation.

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Occupational exposure to vanadium is common in petrochemical, mining, steel, and utilities industries and results in toxic effects largely confined to the respiratory system. Vanadium exposure has been associated with inflammatory changes in the upper and lower respiratory tracts in addition to

Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner.

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BACKGROUND Elevated levels of air pollution are associated with increased risk of lung cancer. Particulate matter (PM) contains transition metals that may potentiate neoplastic development through the induction of oxidative stress and inflammation, a lung cancer risk factor. Vanadium pentoxide

Regulation of chemokine mRNA expression in a rat model of vanadium-induced pulmonary inflammation.

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Environmental and occupational exposure to vanadium dusts results in toxic effects mainly confined to the respiratory system. Using a rat model of acute lung inflammation induced by intratracheal instillation of sodium metavanadate (NaVO3) at the dose of 200 microg V/kg, we investigated the

Modulatory Effect of Concomitant Administration of Insulin and Vanadium on Inflammatory Biomarkers in Type 2 Diabetic Rats: Role of Adiponectin.

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The aim of this study is to investigate the effect of vanadium and/or insulin on the proinflammatory biomarkers in type 2 diabetes mellitus (T2DM) rat model. Sixty male Sprague Dawley rats were divided into six groups (n = 10). Control group, control vanadium group, T2DM group, insulin-treated

Expression and regulation of macrophage inflammatory protein-2 gene by vanadium in mouse macrophages.

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Environmental and occupational exposure to vanadium (V) dusts results in inflammation mainly confined to the respiratory tract. Macrophages apparently play an important role in mediating the inflammation via the production of many chemokines. In the current study, we investigated whether vanadium

Role of neutrophil apoptosis in vanadium-induced pulmonary inflammation in mice.

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Pulmonary exposure to airborne vanadium and vanadium-containing compounds is associated with acute pulmonary inflammation, characterized by a rapid influx of neutrophilic polymorphonuclear leukocytes with a peak response at 6 hours and resolution by 3 days. We hypothesized that neutrophil apoptosis

Anti-inflammatory effects of vanadium-binding protein from Halocynthia roretzi in LPS-stimulated RAW264.7 macrophages through NF-κB and MAPK pathways.

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Vanadium-binding protein (VBP) was separated from the blood of the fresh sea urchin Halocynthia roretzi through (NH₄)₂SO₄ precipitation, Diethylaminoethyl Sepharose fast-flow ion-exchange chromatography, and Sephacryl S-200 high-resolution size-exclusion

Vanadium-induced apoptosis and pulmonary inflammation in mice: Role of reactive oxygen species.

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Pulmonary exposure to metals and metal-containing compounds is associated with pulmonary inflammation, cell death, and tissue injury. The present study uses a mouse model to investigate vanadium-induced apoptosis and lung inflammation, and the role of reactive oxygen species (ROS) in this process.

Respiratory syncytial virus infection reduces lung inflammation and fibrosis in mice exposed to vanadium pentoxide.

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BACKGROUND Vanadium pentoxide (V2O5) exposure is a cause of occupational bronchitis and airway fibrosis. Respiratory syncytial virus (RSV) is a ubiquitous pathogen that causes airway inflammation. It is unknown whether individuals with pre-existing respiratory viral infection are susceptible to

Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice.

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Vanadium is a potentially toxic environmental pollutant and induces oxidative damage in biological systems including the central nervous system (CNS). Its deposition in brain tissue may be involved in the pathogenesis of certain neurological disorders which after prolonged exposure can culminate

Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

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This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed

Platinum levels in nasal lavage fluid as a biomarker for traffic-related exposure and inflammation in children.

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Platinum (Pt) is a well-known constituent of particles emitted by catalytic converters during car operation. To evaluate Pt as a potential marker for traffic related particle exposure, we investigated Pt content along with metals vanadium (V) and chromium (Cr) in coarse and fine particulate matter

Peracute vanadium toxicity in cattle grazing near a vanadium mine.

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Animals may act as bioindicators for potential human health problems associated with mining and refining. Eight cattle died after a vanadium mine dam collapsed close to the area in which they were grazing. Necropsies were conducted on five cattle. Affected animals had shown a watery bloody diarrhea,

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