Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An enzyme immunoassay has been developed to measure human manganese-superoxide dismutase (Mn-SOD) in serum and urine. The assay can be done in less than 5 h, is highly sensitive (detecting limit, 0.1 ng of Mn-SOD) and simple. There is no interference from factors in serum or urine under assay conditions, and the method is specific for human Mn-SOD. Serum Mn-SOD concentrations were markedly increased in patients with liver diseases, but not in renal diseases. On the other hand, urinary Mn-SOD levels were elevated in a few patients with nephrotic syndrome and lung cancer, but were decreased in patients with hypertension. Furthermore, investigations were conducted on the clinical course of serum Mn-SOD levels in a case of alcoholic hepatitis, and on correlations between serum Mn-SOD and the conventional liver function tests. The localization of Mn-SOD in liver was also explored using immunofluorescent staining. The fluorescence was intense in the degenerated portions of liver tissue from a patient with drug-induced hepatitis.
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PMID:Enzyme immunoassay for manganese-superoxide dismutase in serum and urine. 676 11

The squamous cell carcinoma of lung was induced with methylcholanthrene (MCA) in iodized oil in Wistar rats. During the development of the cancer, the animals were given superoxide dismutase (SOD) or its inhibitor diethyldithiocarbamate (DDC). In DDC group, 3 out of 50 rats developed cancer and 4 developed atypical hyperplasia of bronchial epithelium within 35 to 40 days. In SOD group, no cancer developed in all of the 52 rats, and only one had atypical hyperplasia in the lungs. Only one of 42 control rats had cancer and 2 rats had atypical hyperplasia of bronchial epithelium. The difference in cancer frequency between groups DDC and SOD was significant (P < 0.05). The results suggest that there is a synergism between DDC and MAC in the induction of lung cancer, while SOD can inhibit MCA-induced lung cancer development. The mechanism of the effect of SOD and DDC was discussed.
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PMID:[Effect of superoxide dismutase and diethyldithiocarbamate on the induction of squamous cell carcinoma of lung with methylcholanthrene in rats]. 780 55

We focused here on steady-state mRNA levels of genes involved in antioxidant defense, i.e., manganese superoxide dismutase and copper-zinc superoxide dismutase, and in cell proliferation, i.e., ornithine decarboxylase, c-jun, and glyceraldehyde-3-phosphate-dehydrogenase in whole-lung homogenates from Fischer 344 rats at 3 h to 20 d after exposure to crocridolite asbestos. Changes in gene expression were correlated with histopathologic findings, total and differential cell counts in bronchoalveolar lavage, and levels of hydroxyproline in lung. Dosage-dependent increases in mRNA levels of antioxidant enzymes and proliferation-related genes were observed. Differential cell counts revealed a dose-related infiltration of neutrophils that preceded elevations in gene expression. Neutrophil infiltration into lung and focal lesions of fibrosis as well as increased levels of hydroxyproline were observed only at high concentrations of asbestos. These results indicate that high airborne concentrations of asbestos cause molecular changes in lung that may be related to antioxidant defense and the triggering of cell proliferation, a feature of asbestosis and lung cancer.
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PMID:Dose-responsive increases in pulmonary fibrosis after inhalation of asbestos. 802 51

Occupational exposure to silica has often been associated with the development of pulmonary fibrosis and, occasionally, lung cancer. Their development may be mediated by oxidant-induced cellular injury. The short- and long-term effects of a single intratracheal instillation of silica in rats (10 mg/200 microliters/saline per rat) was assessed by measuring 8-hydroxy-2'-deoxyguanosine (oh8dG) levels in lung tissue and peripheral blood leukocytes. Cell differentials, reduced glutathione (GSH), and superoxide dismutase (SOD), lipid peroxide, and total phospholipids in peripheral blood and/or bronchoalveolar lavage fluid (BALF) were also measured. The pulmonary oh8dG levels increased approximately 2.24- 2.86-fold from 1 to 5 days after exposure to silica. It was still elevated 1 and 4 weeks after installation, but the difference was no longer statistically significant. The oh8dG levels in peripheral blood leukocytes were never significantly different, but they were generally higher than in the controls. The low SOD levels in the BALF of exposed rats in the early stage and the higher GSH levels in the late stage may represent protective reactions against the generation of oxygen species. A significant increase in oh8dG levels in lung tissue suggested the possible carcinogenicity of silica.
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PMID:Oxidative DNA damage induced by silica in vivo. 860 69

This investigation was effected to determine the levels of the two antioxidant enzymes, superoxide dismutase (SOD) (EC 1.15.1.1) and catalase (CAT) (EC 1.11.1.6) in lung cancerous tissues and to compare with normal lung tissue in order to evaluate the antioxidant status in lung cancer. Fifteen lung carcinoma tissue samples and the normal counterparts from the same cases were homogenized and the cytosols obtained by ultracentrifugation (100,000 x g). SOD was assayed using a modification of the indirect nitroblue tetrazolium assay method, while CAT was measured by a spectrophotometric method. The data obtained are as follows: 1.42 +/- 0.24 U/mg protein (means +/- SEM) of SOD in lung cancer and 3.13 +/- 0.51 U/mg protein in normal lung tissue and 33.53 +/- 6.09 U/mg protein of CAT in lung cancer and 71.33 +/- 14.38 in normal lung tissue. The differences were found to be significant at the level of P < 0.01 for both enzymes. These low levels of the antioxidant enzymes in lung cancerous tissues can lead to elevated levels of reactive oxygen metabolites, resulting in damage to the key subcellular structures such as DNA, cell membranes, and other vital cellular components.
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PMID:Evaluation of some antioxidant enzymes in lung carcinoma tissue. 863 62

Nicotine, a major component of cigarette smoke, plays an important role in the development of cardiovascular disease and lung cancer in smokers. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis and the level of lipid peroxides is increased in smokers. In rats fed a high-fat diet, the tissue concentration of lipid peroxides was found to be increased. On nicotine administration along with a high-fat diet an additive effect was observed in lipid peroxidation and free radical scavengers. The activities of scavenging enzymes superoxide dismutase, catalase and glutathione reductase were found to be decreased, while the glutathione concentration and activity of glutathione peroxidase were enhanced.
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PMID:Effect of nicotine on antioxidant defence mechanisms in rats fed a high-fat diet. 884 84

Cigarette smoking has been established as a major risk factor for atherosclerosis and also for lung cancer. Nicotine is one of the major toxic components of cigarette smoke that is believed to be partly responsible for the deleterious effect of cigarette smoke. Alcohol intake is another major risk factor for the development of cardiovascular disease. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis. The concentration of lipid peroxides is found to be increased in alcohol-treated rats. On nicotine administration along with alcohol, an additive effect was observed in lipid peroxidation and the antioxidant defence mechanism. The activity of scavenging enzymes superoxide dismutase, catalase and glutathione reductase was found to be decreased, while the activity of glutathione peroxidase and the concentration of glutathione were increased.
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PMID:Additive effect of alcohol and nicotine on lipid peroxidation and antioxidant defence mechanism in rats. 885 16

Glutathione (GSH) is one of the key components of the lung antioxidant defenses. Chronic smokers have higher GSH concentrations in their epithelial lining fluid than do nonsmokers. The aim of this study was to compare antioxidant concentrations in epithelial lining fluid (ELF) from nonsmokers, smokers with, and smokers without non-small-cell lung cancer. The study found that GSH in ELF from patients with lung cancer was significantly greater than in ELF from smokers and nonsmokers, at 1,485.5 +/- 208, 544 +/- 97.6 microM, and 339.3 +/- 112 microM, respectively (p < 0.05). In contrast, superoxide dismutase (SOD) was lower in ELF from patients with lung cancer than in that from smokers and nonsmokers, at 3.52 +/- 0.99, 30.82 +/- 8.2, and 43.91 +/- 10.1 U/ml, respectively (p < 0.05). Spontaneous superoxide anion release by adherent alveolar macrophages (AM) showed no difference between smokers with and without lung cancer. These data indicate that patients with lung cancer have marked modifications in their ELF antioxidant defenses by comparison with those of smokers. It is difficult to distinguish whether changed antioxidant status is a primary disturbance involved in the cancer process or whether it is a consequence of the neoplastic changes in malignancy.
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PMID:Antioxidant activity in bronchoalveolar lavage fluid from patients with lung cancer. 897 Mar 59

Cigarette smoking has been shown to be a major risk factor for cardiovascular disease, lung cancer, and respiratory diseases. Due to its high content of oxidants, the cigarette smoke is bound to cause a prooxidant/antioxidant imbalance in the blood plasma and tissues of smokers. The study groups were selected from an apparently healthy population living in urban areas, comprising 200 subjects aged 18 to 80 years, half of whom were smokers. In smokers aged 18 to 45 years, the changes of the plasma prooxidant parameters (i.e., lipid peroxides, leukocyte activation, and the antioxidant ones [thiol concentration, total antioxidant capacity]) were not significantly different from those of the age-matched controls, whereas in the 46 to 80 age group they were. In smokers, both antioxidant erythrocyte enzymes, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), exhibited increased activity in the 18 to 45 age group and decreased activity in the 46 to 80 age group. The differences in enzyme activity between the smoking and nonsmoking groups were highly significant for SOD in all ages, whereas for GSH-Px the difference in activity was significant only in the case of older smokers. These findings would suggest that a process of adaptation takes place in younger smokers, in whom the antioxidant systems are able to counteract the oxidant factors, while in older smokers this process is no longer occurring and the plasma and tissues are under permanent oxidative stress. Our results clearly demonstrated that a prooxidant/antioxidant imbalance exists in the blood of smokers, and the determination of leukocytes stimulation index may be a useful and simple way of assessing the oxidative stress status of these individuals. A hypothesis regarding a possible mechanism linking cigarette smoking to the development of coronary heart disease is presented.
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PMID:Cigarette smoking causes biochemical changes in blood that are suggestive of oxidative stress: a case-control study. 900 95

Cross-resistance presents an obstacle in cancer chemotherapy. Cadmium is a potential carcinogen whose exposure has been shown in epidemiological and laboratory experiments to cause lung cancer. Cadmium also induces various forms of resistance in human lung carcinoma cells. This resistance may be shared by antineoplastic agents, which should be a concern for chemotherapy of cadmium-induced lung cancer. In the present study, two subpopulations of human lung carcinoma A549 cells with a different magnitude of resistance to cadmium toxicity were shown to have a parallel resistance to the cytotoxic action of Adriamycin (ADR), an important anticancer drug. Several factors were examined to investigate the mechanism(s) for the cross-resistance, including cellular metallothionein and glutathione (GSH) concentrations, glutathione S-transferase activity, mdr1 expression, and antioxidant enzyme activities including superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. Only cellular GSH content was elevated consistently in the cadmium/ADR-resistant cells relative to the cadmium/ADR-sensitive cells. Treatment with buthionine sulfoximine, a specific inhibitor of GSH synthesis sensitized both cell lines to ADR only when the cellular GSH levels were depleted to about 5% of control. This BSO treatment, however, did not affect cell viability. Further study revealed that the cadmium/ADR-resistant cells have a greater capacity in recovery of cellular GSH content following BSO treatment. The results demonstrate that cross-resistance to ADR exists in cadmium-resistant human lung carcinoma A549 cells, and enhanced GSH synthesis capacity, rather than elevated levels of cellular GSH, may be related to this resistance.
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PMID:Decreased sensitivity to adriamycin in cadmium-resistant human lung carcinoma A549 cells. 911 95


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