Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glutathione (GSH) is an important constituent in protecting the cellular elements within the lower respiratory tract against oxydants. We measured GSH in bronchoalveolar lavage fluid (BAL) in twelve patients with lung fibrosis and compared the data to eight healthy controls. GSH in BAL was 0.71 +/- 0.34 mumol/l in patients with lung fibrosis and 0.88 +/- 0.35 mumol/l in the controls (p greater than 0.05). After relating GSH on the volume of the epithelial lining fluid (ELF), determined by the urea method, GSH/ELF was 93 +/- 71 mumol/l in lung fibrosis and significantly different (p less than 0.005) from 387 +/- 240 mumol/l in the controls. In seven patients (four lung fibrosis, one desquamative pneumonitis, two asbestosis) GSH in BAL was determined before and after seven days of medication with 1800 mg N-acetylcysteine/day. We observed a significant increase of GSH in BAL from 0.93 +/- 0.46 to 1.56 +/- 0.92 mumol/l. Our observations confirm that in patients with lung fibrosis the protective ability against oxydants is diminished and that one parameter of the antioxydative capacity (GSH) can be increased in BAL by oral administration of N-acetylcysteine. Further studies are necessary to investigate the clinical and therapeutic implications of our findings.
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PMID:[The effect of oral N-acetylcysteine on glutathione concentration in bronchoalveolar lavage of patients with fibrosing lung diseases]. 188 13

After instillation of cadmium (Cd) into the rat trachea, reduced and oxidized glutathione (GSH and GSSG) levels in the lung, liver and kidney were studied in relation to Cd concentrations and metallothionein (Mt) contents. Rats instilled with Cd developed haemorrhagic pneumonia, which deteriorated with a marked swelling of the lung throughout the experimental period of 48 h. The total glutathione (GSH + GSSG) level in the organs decreased after 6 h to 60-70% of the control levels. The decreased glutathione level was never restored to the control level within 48 h in the lung, and was possibly due to the pneumonia. Completely recovered glutathione was seen in other organs. The GSSG level did not decrease significantly in the lung or liver but lowered significantly after 12 h and 24 h. The GSSG fraction in the amount of total glutathione was 10% or more in the lung and 5% or less in the liver or kidney. This finding indicated that the total glutathione level was mainly changed by the decrease in the GSH fraction. Cadmium in the lung increased to 7.3 ppm 3 h after Cd instillation and decreased to 2.5 ppm within 48 h. Cadmium in the liver and kidney gradually increased with time, and after 48 h reached 1.1 and 2.3 ppm, respectively. This indicated a transportation of Cd from the lung to these organs. Moreover, the early stage of Cd accumulation coincided with the total glutathione decrease in the organs. After Cd instillation, pulmonary, hepatic and renal Mt started to increase at 3 or 6 h, and markedly increased at 24 h or later.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early decreases in pulmonary, hepatic and renal glutathione levels in response to cadmium instillation into rat trachea. 191 96

Radiation pneumonitis are well recognized as complications of radiotherapy for the thoracic malignancies. However, the pathogenesis of radiation pneumonitis has been poorly understood and prevention of it has not been developed. In this study, to define the mechanisms of radiation pneumonitis biologically, we measured lipid peroxides, the activities of glutathione peroxidase (GSH pex.), leukotriene C4 and D4 (LTC4 and LTD4) in the irradiated lungs of mice. Eight weeks old female ICR mice were sacrificed at various time periods (immediately after to 5 days) following the 10 Gy whole-body irradiation with 60Co gamma rays. The lipid peroxides and the activities of GSH pex. increased immediately after the irradiation, but returned to the control level 1 hour after the irradiation. And then, the lipid peroxides also increased from 1 day after the irradiation, while the activities of GSH pex. decreased below the control level. LTC4 and LTD4 in the irradiated lungs of mice were also significantly higher than those of non-irradiated controls. Furthermore, we investigated effects of Coenzyme Q10 and Azelastine for the prevention of radiation pneumonitis. Lungs of ICR mice after 10 Gy whole-thorax irradiation treated with those drugs were compared with the control lungs pathologically. Intraperitoneal administration of those drugs decreased the damages for endothelium, such as vacuole formation and stripping off the basement membrane which were recognized by electron microscope. Based on these results, it was strongly suggested that initial damage of irradiated lungs might be induced by lipid peroxides and leukotrienes, and that Coenzyme Q10 and Azelastine could reduce radiation pneumonitis.
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PMID:[Experimental studies on mechanisms and prevention of radiation pneumonitis]. 275 99

Dramatic haemolysis may accompany viral hepatitis and pneumococcal pneumonia in G6PD-deficient patients. Since red blood cells (RBCs) are richly endowed with receptors for activated complement, particularly C3b, we hypothesized that bulky, complement-activating immune complexes (IC) consisting of microbes and antibody might attract granulocytes (PMNs), facilitating oxidative 'innocent bystander' RBC damage. Indeed, opsonization with only two type-2 pneumococcus (PN3)/anti-PN3/C3b complexes per RBC caused agglutination of RBC, a phenomenon termed immune adherence. Addition of as few as one PMN per 20 opsonized RBCs caused the glutathione (GSH) levels of co-incubated G6PD-deficient RBCs to fall by 30% (from 3.5 to 1.8 +/- 0.8 mumoles GSH/g Hb) compared to identically incubated, but nonopsonized, G6PD-deficient RBCs. GSH levels remained normal (5.2 +/- 0.4 mumoles/g Hb) in PMN-exposed opsonized normal RBCs. GSH depletion in G6PD-deficient RBC was directly related to disease severity--falling a mean 33% in RBCs from two Black G6PD A- subjects but 59% in two Caucasian G6PD deficient RBCs. Prevention of C3b generation (with 10 mM EDTA) during opsonization abrogated both immune adherence and PMN-mediated GSH decline in oxidant-sensitive cells. Similarly, removal of C3b receptors by brief trypsin incubation of RBCs eliminated immune adherence and GSH decline. Thus, both phenomena are dependent on IC complement activation and subsequent binding of the bacterial IC to the RBC complement receptors. Although clearance of IC by RBCs may be beneficial in protecting other tissues from inflammatory damage, G6PD-deficient RBCs are vulnerable to oxidants generated by juxtaposed phagocytes--cells attracted to, and stimulated by, the immune complex/C3b combination. It is suggested that this 'Good Samaritan' activity of RBCs may lead to haemolysis during periods of exuberant antibody response to microbes.
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PMID:G6PD-deficiency infectious haemolysis: a complement dependent innocent bystander phenomenon. 370 64

The present study was carried out in order to examine the efficiency of selenium/vitamin E on the health status in the first eight weeks of life in Se-deficient neonate calves. The experiments were done with 54 calves from two farms. Animals with low selenium level p.n. (< 40 micrograms/l) were randomly classified alternatively to be treated (gr. I) or to serve as control (gr. II). The calves of group I were treated with 0.2 mg selenium and 60 mg vitamin E per kg body weight subcutaneously on the first and third day p.n.; they got another treatment with half of the dosage in the fourth week of life. Group II received a placebo (0.9% sterile NaCl-solution). Clinical and haematological examination brought following results: Group I showed a lower infection rate and the duration of infection (especially in the case of pneumonia) was shorter than in the controls. During two days, after initial selenium substitution, the GSH-Px-activity was clearly higher in the animals of group I. The amount of antibiotics and special diets per calf was lower in group I. In conclusion it can be said, that the application of selenium and vitamin E seemed to improve the status of health in the Se-deficient calves, although the results could not be assured statistically.
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PMID:[Effects of a selenium/vitamin E substitution on the development of newborn calves on selenium-deficient farms]. 971 Sep 21

In order to investigate the relationship between selenium (Se) status and pneumonia children, the levels of Se and glutathione peroxidase (GSH-Px) in plasma and white blood cells and Se content in urine were determined in 57 cases with pneumonia and 85 control children under 10 years old. The results showed that the levels of Se and GSH-Px in plasma and white blood cell in the group of pneumonia were significantly lower, but the content of Se in urine was higher. Se content and GSH-Px activity in white blood cells of patients during crisis were significantly lower than those of patients during convalescence.
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PMID:[The comparison of selenium status between the children suffered from pneumonia and the normal children from kindergarten]. 1032 95

Among the main characteristics of Legionella pneumophila pneumonia are acute lung injury and severe hypoxemia. Although high oxygen supplementation is a valuable supportive therapy in these patients, oxygen itself is known to be a risk factor for acute lung injury. The effects of hyperoxia on lung injury of mice with Legionella pneumonia were examined. Hyperoxia treatment reduced survival of the infected mice in an oxygen concentration- and exposure time-dependent manner. The enhanced lethality was associated with an increase in total lung weight and apoptosis markers, but not with bacterial burden in the lungs. Hyperoxia decreased the levels of the antioxidant glutathione (GSH) in infected lungs. Exogenous tumour necrosis factor-alpha (TNF-alpha) improved the survival of infected mice kept under hyperoxia. TNF-alpha effects were associated with restoration of total lung weight and histone DNA and GSH levels on day 2, whereas the lung bacterial burden did not differ significantly. Moreover, upregulation of GSH by TNF-alpha was observed in the lungs of mice without infection. These results demonstrate that hyperoxia exacerbates L. pneumophila pneumonia. The data suggest that TNF-alpha may be a potential therapeutic candidate for these individuals, not only through modulating host antibacterial systems, but also by mediating induction of the antioxidant GSH.
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PMID:Legionella-induced acute lung injury in the setting of hyperoxia: protective role of tumour necrosis factor-alpha. 1527 58

In this article, oxidative stress and enzymic-non-enzymic antioxidants status were investigated in children with acute pneumonia. Our study included 28 children with acute pneumonia and 29 control subjects. The age ranged from 2 to 11 years (4.57+/-2.13 years) and 2 to 12 years (4.89+/-2.22 years) in the study and control groups, respectively. Whole blood malondialdehyde (MDA) and reduced glutathione (GSH), serum beta-carotene, retinol, vitamin C, vitamin E, catalase (CAT), ceruloplasmin (CLP), total bilirubin, erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels were studied in all subjects. There was a statistically significant difference between the groups for all parameters except for serum CAT. Whole blood MDA, serum CLP and total bilirubin levels were higher in the study group than those of the control group. However, SOD, GPx, beta-carotene, retinol, vitamin C, vitamin E and GSH levels were lower in the study group compared with the control group. All antioxidant vitamin activities were decreased in children with acute pneumonia. Our study demonstrated that oxidative stress was increased whereas enzymic and non-enzymic antioxidant activities were significantly decreased in children with acute pneumonia.
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PMID:Oxidative stress and enzymic-non-enzymic antioxidant responses in children with acute pneumonia. 1663 91

Periodic pneumonia outbreaks cause large-scale die-offs that threaten the viability of bighorn sheep (Ovis canadensis) populations. Bighorns are highly susceptible to pneumonia, and in some cases this susceptibility may be exacerbated by trace mineral deficiencies. To evaluate responses to injectable selenium supplementation, eight captive bighorn sheep were treated with either an injectable sodium selenite supplement or a saline control. We collected 6-ml blood aliquots before and at 1, 6, and 12 wk posttreatment. We submitted one set of aliquots immediately to measure selenium (Se) and zinc (Zn) concentrations and glutathione-peroxidase (GSH-Px) activity; additional aliquots were held at about 22 C and then submitted at 1, 3, and 7 days postcollection to assess effects of storage on these measures. Neither Se nor GSH-Px were affected by selenite injections. Both Se and GSH-Px demonstrated small linear decays over the 7-day storage period (0.011 ppm/day [SE=0.0027] and 15.78 mmole/l/sec/day [SE=6.88], respectively); in contrast, Zn concentrations in stored samples increased logarithmically (0.35 ppm/day on the natural log scale). Blood Se and GSH-Px were not correlated in sampled bighorns; however, because all values for both measures were within normal limits, lack of correlation did not affect interpretation of these data in our study.
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PMID:Effects of selenium supplementation and sample storage time on blood indices of selenium status in bighorn sheep. 1961 91

Excessive alcohol use increases the risk of acute lung injury and pneumonia. Chronic alcohol ingestion causes oxidative stress within the alveolar space, including near depletion of glutathione (GSH), which impairs alveolar epithelial and macrophage function, in experimental animals and human subjects. However, the fundamental mechanism(s) by which alcohol induces such profound lung oxidative stress is unknown. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a redox-sensitive master transcription factor that regulates activation of the antioxidant response element (ARE). As the alveolar epithelium controls GSH levels within the alveolar space, we hypothesized that alcohol also decreases Nrf2 expression and/or activation within the alveolar epithelium. In this study, we determined that alcohol ingestion in vivo or direct alcohol exposure in vitro down-regulated the Nrf2-ARE pathway in lung epithelial cells, decreased the expression of antioxidant genes, and lowered intracellular GSH levels. RNA silencing of Nrf2 gene expression in alveolar epithelial cells in vitro decreased expression of these same antioxidant genes, and likewise lowered intracellular GSH levels, findings that mirrored the effects of alcohol. In contrast, treating alcohol-exposed alveolar epithelial cells in vitro with the Nrf2 activator, sulforaphane, preserved Nrf2 expression, ARE activation, intracellular GSH levels, and epithelial barrier function. These new experimental findings implicate down-regulation of the Nrf2-ARE signaling pathway as a fundamental mechanism by which alcohol causes profound oxidative stress and alveolar epithelial dysfunction, and suggest that treatments, such as sulforaphane, that activate this pathway could mitigate the pathophysiological consequences of alcohol on the lung and other organs.
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PMID:Alcohol causes alveolar epithelial oxidative stress by inhibiting the nuclear factor (erythroid-derived 2)-like 2-antioxidant response element signaling pathway. 2330 37


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