pneumoconiosis/glutathione

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Decreased glutathione content and glutathione S-transferase activity in red blood cells of coal miners with early stages of pneumoconiosis.

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Blood samples of miners heavily exposed to coal dust were examined for changes in glutathione S-transferase (GST) activity. Decreased GST activity was found in red blood cells of subjects with early stages of coal workers' pneumoconiosis (International Labour Office classification 0/1-1/2) when

Miners compensated for pneumoconiosis and glutathione s-transferases M1 and T1 genotypes.

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Chronic inhalation of quartz-containing dust produces reversible inflammatory changes in lungs resulting in irreversible fibrotic changes termed pneumoconiosis. Due to the inflammatory process in the lungs, highly reactive substances are released that may be detoxified by glutathione S-transferases.

Cross sectional and longitudinal study on selenium, glutathione peroxidase, smoking, and occupational exposure in coal miners.

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OBJECTIVE To understand the variations of selenium (Se) concentration relative to changes in occupational exposure to coal dust, taking into account age and changes in smoking habits in miners surveyed twice, in 1990 and 1994. To better understand the relation of Se concentration with glutathione

Inherited glutathione-S-transferase deficiency is a risk factor for pulmonary asbestosis.

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Pulmonary diseases attributable to asbestos exposure constitute a significant public health burden, yet few studies have investigated potential genetic determinants of susceptibility to asbestos-related diseases. The glutathione-S-transferases are a family of conjugating enzymes that both catalyze

Blood anti-oxidant parameters at different stages of pneumoconiosis in coal workers.

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The pneumoconioses are associated with chronic inflammatory processes during which increased amounts of reactive oxygen species are formed in the lower respiratory tract. To characterize the effect(s) of these processes on the defense system against free radicals, we studied 91 individuals with

Chemical reactivity of the carbon-centered free radicals and ferrous iron in coals: role of bioavailable Fe2+ in coal workers pneumoconiosis.

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Striking differences in the prevalence of coal workers' pneumoconiosis (CWP) exist between different coal mine regions. The major factors responsible for the observed regional differences in CWP have not yet been identified. In the present study, chemical reactivity of the carbon-centered free

Antioxidant response at early stages and low grades of simple coal worker's pneumoconiosis diagnosed by high resolution computed tomography.

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In miners exposed to coal dusts, coal worker's pneumoconiosis (CWP) can occur. The purpose of the present study is to better understand the relations between coal dust exposure and activities of blood plasma antioxidant enzymes, namely, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px),

Serum and BAL cytokine and antioxidant enzyme levels at different stages of pneumoconiosis in coal workers.

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Coal workers' pneumoconiosis (CWP) is an occupational pulmonary disease that occurs by chronic inhalation of coal dust. CWP is divided into two stages depending on the extent of the disease, as simple pneumoconiosis (SP) and progressive massive fibrosis (PMF). In the present study, serum and

Mechanistically identified suitable biomarkers of exposure, effect, and susceptibility for silicosis and coal-worker's pneumoconiosis: a comprehensive review.

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Clinical detection of silicosis is currently dependent on radiological and lung function abnormalities, both late manifestations of disease. Markers of prediction and early detection of pneumoconiosis are imperative for the implementation of timely intervention strategies. Understanding the

Evaluation of the exposure to coal dust and prevalence of pneumoconiosis in underground mining in three Colombian departments

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Introduction: Coal workers’ pneumoconiosis is a chronic and irreversible disease representing a public health problem.Objective: To estimate the prevalence of pneumoconiosis and its associated factors among underground coal miners in the Colombian departments of Boyacá, Cundinamarca and Norte de

Effect of TNF and LTA polymorphisms on biological markers of response to oxidative stimuli in coal miners: a model of gene-environment interaction. Tumour necrosis factor and lymphotoxin alpha.

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BACKGROUND Interaction between genetic background and oxidative environmental stimuli in the pathogenesis of human lung disease has been largely unexplored. METHODS A prospective epidemiological study was undertaken in 253 coal miners. Intermediate quantitative phenotypes of response to oxidant

Examination of lung toxicity, oxidant/antioxidant status and effect of erdosteine in rats kept in coal mine ambience.

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Occupational exposure to coal dust causes pneumoconiosis and other diseases. Reactive oxygen species (ROS) have been implicated in the pathogenesis of coal dust-induced lung toxicity. In this experimental study, we investigated the oxidant/antioxidant status, nitric oxide (NO) and hydroxyproline

Blood antioxidant enzymes as markers of exposure or effect in coal miners.

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OBJECTIVE To investigate if blood Cu++/Zn++ superoxide dismutase, glutathione peroxidase, catalase, and total plasma antioxidant activities could be markers of biological activity resulting from exposure to respirable coal mine dust in active miners, and of pneumoconiosis in retired

Changes in bronchoalveolar lavage indices associated with radiographic classification in coal miners.

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Previous studies on symptomatic coal miners have shown that alveolar macrophages, recovered by bronchoalveolar lavage (BAL), release excessive amounts of reactive oxygen species (ROS) and inflammatory cytokines. It has been proposed that these secretions may mediate cell injury and initiate the

[The influence of dust and heating microclimate on lipid peroxidation].

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In experimental pneumoconiosis both under normal and heating ambient temperature lipid peroxidation is not activated, although heating microclimate increases alteration of lung tissue and induces rapid and intensive pulmonary fibrosis. Association of dust and heating microclimate prolongs a period

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