High Levels of Catalase and Glutathione Peroxidase Activity Dampen H<sub>2</sub>O<sub>2</sub>Signaling in Human Alveolar Macrophages

Carter, A. Brent; Tephly, Linda A.; Venkataraman, Sujatha; Oberley, Larry W.; Zhang, Yuping; Buettner, Garry R.; Spitz, Douglas R.; Hunninghake, Gary W.

doi:10.1165/rcmb.2003-0377oc

Cited by 61 publications

(58 citation statements)

References 78 publications

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“…Enzymatic parameters of oxidative stress results in this study showed no significant difference in CAT and GST activity means between the exposed and non-exposed groups (Table 3), nor between individuals exposed without asbestosis and those exposed with asbestosis (Table 4), in contrast to previous observations in the international literature [35][36][37].…”

Section: Group Exposed To Asbestoscontrasting

confidence: 99%

“…It is possible that this same effect occurred with the CAT activity too; however, an increase in CAT activity induced by asbestos fibers has been reported in the literature, but did not compare exposed individuals without and with asbestosis [36,37]. Furthermore, a positive statistically significant correlation (p < 0.001, R = + 0.527) was found between the CAT results with GST, using partial correlation, controlled by age, smoking habits and alcohol consumption.…”

Section: Group Exposed To Asbestosmentioning

confidence: 86%

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Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Amaral¹,

Joca²,

Carvalho³

et al. 2016

Biomonitoring

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group and individuals without asbestosis, respectively. Linear regression analysis showed that 28,4% and 50,5% of comet assay results were increased by exposure to asbestos and developed asbestosis. The results of CAT and GST were not difference between the groups. These results supports the association of genotoxic damage and the onset of asbestosis by chrysotile asbestos exposure in workers of this study.Keywords: asbestos, occupational exposure, genotoxicity. IntroductionAsbestosis is a form of pneumoconiosis caused by inhaling asbestos, a generic commercial designation for a group of naturally-occurring mineral silicate fibres of the serpentine (chrysotile asbestos) and amphibole series (actinolite, amosite, anthophyllite, crocidolite and tremolite) [1]. Inhaling any kind of asbestos fibers causes the development of intense interstitial pulmonary fibrosis, which involves an inflammatory reaction, production of collagen and the formation of granuloma [2][3][4][5].Asbestosis and other diseases related to asbestos are increasing worldwide [6,7] and several studies have shown that exposure to asbestos has contributed to occupationally-related cancer. Each year, approximately 125 million people around the world are occupationally exposed to asbestos and at least 100,000 people die because of diseases related to this exposure (for example asbestos-related lung cancer, mesothelioma, or asbestosis [1]) despite the fact that "chrysotile manufacturers, governments of asbestos-producing nations, and some asbestos miners' unions contend either that their products do not cause disease or that there is insufficient evidence to reach a reliable conclusion", as stated by Pezerat (2009) [8]. Abstract: Genotoxic effects of occupational workers exposed to asbestos can be evaluated using different biomarkers as oxidative stress enzymes in conjuction with comet assay. This study assessed changes to oxidative stress enzymatic parameters and genotoxic damage in workers occupationally exposed and non-exposed to chrysotile asbestos, who attended the outpatient Clinic of the Center for Worker Health Studies and Human Ecology (CESTEH/ENSP/FIOCRUZ) in Brazil. Chest radiography and spirometry were performed to assess clinical progression of symptoms. The traditional visual score comet assay in peripheral whole blood cells was used to assess DNA damage, and oxidative stress was evaluated by measuring catalase (CAT) and glutathione S-transferase (GST) activities. Respiratory alterations were observed in 53% of workers exposed, as determined by pulmonary function and bronchodilation, and 6 workers were diagnosed with asbestosis. The comet assay was statistically significantly higher in the exposed group and individuals with asbestosis compared to the non-exposed

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Section: Group Exposed To Asbestoscontrasting

confidence: 99%

Section: Group Exposed To Asbestosmentioning

confidence: 86%

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Amaral¹,

Joca²,

Carvalho³

et al. 2016

Biomonitoring

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“…It also has been shown that inhibition of catalase by 3-AT increases H 2 O 2 levels in macrophages (54). NO may attenuate H 2 O 2 production by inducing catalase.…”

Section: Discussionmentioning

confidence: 96%

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Yoshioka

Kitao

Kishino

et al. 2006

The Journal of Immunology

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We investigated the cytoprotective effect of NO on H2O2-induced cell death in mouse macrophage-like cell line RAW264. H2O2-treated cells showed apoptotic features, such as activation of caspase-9 and caspase-3, nuclear fragmentation, and DNA fragmentation. These apoptotic features were significantly inhibited by pretreatment for 24 h with NO donors, sodium nitroprusside and 1-hydroxy-2-oxo-3,3-bis-(2-aminoethyl)-1-triazene, at a low nontoxic concentration. The cytoprotective effect of NO was abrogated by the catalase inhibitor 3-amino-1,2,4-triazole but was not affected by a glutathione synthesis inhibitor, l-buthionine-(S,R)-sulfoximine. NO donors increased the level of catalase and its activity in a concentration-dependent manner. Cycloheximide, a protein synthesis inhibitor, inhibited both the NO-induced increase in the catalase level and the cytoprotective effect of NO. These results indicate that NO at a low concentration protects macrophages from H2O2-induced apoptosis by inducing the production of catalase.

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“…For histology sections, similar thymic lobes were fixed in formalin, embedded in paraffin, cut in 5-Am sections, and stained with H&E. In-gel (nondenaturing PAGE) enzyme assay was used to determine the activities of superoxide dismutases (SOD) and catalase. The achromatic band intensities indicated the enzyme activities (27).…”

Section: Methodsmentioning

confidence: 99%

Tumor-Induced Oxidative Stress Perturbs Nuclear Factor-κB Activity-Augmenting Tumor Necrosis Factor-α–Mediated T-Cell Death: Protection by Curcumin

et al. 2007

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Cancer patients often exhibit loss of proper cell-mediated immunity and reduced effector T-cell population in the circulation. Thymus is a major site of T-cell maturation, and tumors induce thymic atrophy to evade cellular immune response. Here, we report severe thymic hypocellularity along with decreased thymic integrity in tumor bearer. In an effort to delineate the mechanisms behind such thymic atrophy, we observed that tumor-induced oxidative stress played a critical role, as it perturbed nuclear factor-KB (NF-KB) activity. Tumor-induced oxidative stress increased cytosolic IKBA retention and inhibited NF-KB nuclear translocation in thymic T cells. These NF-KB-perturbed cells became vulnerable to tumor-secreted tumor necrosis factor (TNF)-A (TNF-A)-mediated apoptosis through the activation of TNF receptorassociated protein death domain-associated Fas-associated protein death domain and caspase-8. Interestingly, TNF-Adepleted tumor supernatants, either by antibody neutralization or by TNF-A-small interfering RNA transfection of tumor cells, were unable to kill T cell effectively. When T cells were overexpressed with NF-KB, the cells became resistant to tumor-induced apoptosis. In contrast, when degradationdefective IKBA (IKBA super-repressor) was introduced into T cells, the cells became more vulnerable, indicating that inhibition of NF-KB is the reason behind such tumor/TNF-Amediated apoptosis. Curcumin could prevent tumor-induced thymic atrophy by restoring the activity of NF-KB. Further investigations suggest that neutralization of tumor-induced oxidative stress and restoration of NF-KB activity along with the reeducation of the TNF-A signaling pathway can be the mechanism behind curcumin-mediated thymic protection. Thus, our results suggest that unlike many other anticancer agents, curcumin is not only devoid of immunosuppressive effects but also acts as immunorestorer in tumor-bearing host.

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High Levels of Catalase and Glutathione Peroxidase Activity Dampen H₂O₂Signaling in Human Alveolar Macrophages

Cited by 61 publications

References 78 publications

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Tumor-Induced Oxidative Stress Perturbs Nuclear Factor-κB Activity-Augmenting Tumor Necrosis Factor-α–Mediated T-Cell Death: Protection by Curcumin

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High Levels of Catalase and Glutathione Peroxidase Activity Dampen H2O2Signaling in Human Alveolar Macrophages

Cited by 61 publications

References 78 publications

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Nitric Oxide Protects Macrophages from Hydrogen Peroxide-Induced Apoptosis by Inducing the Formation of Catalase

Tumor-Induced Oxidative Stress Perturbs Nuclear Factor-κB Activity-Augmenting Tumor Necrosis Factor-α–Mediated T-Cell Death: Protection by Curcumin

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High Levels of Catalase and Glutathione Peroxidase Activity Dampen H₂O₂Signaling in Human Alveolar Macrophages