DNA damage and cellular abnormalities in tuberculosis, lung cancer and chronic obstructive pulmonary disease

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Background

Tuberculosis (TB), Lung Cancer (LC) and Chronic Obstructive Pulmonary Diseases (COPD) affect millions of individuals worldwide. Monitoring of DNA damage in pathological situations has been investigated because it can add a new dimension to clinical expression and may represent a potential target for therapeutic intervention. The aim of this study was to evaluate DNA damage and the frequency of cellular abnormalities in TB, LC and COPD patients by comparing them to healthy subjects.

Methods

The detection of DNA damage by a buccal micronucleus cytome assay was investigated in patients with COPD ( n = 28), LC ( n = 18) and TB ( n = 22) and compared to control individuals ( n = 17).

Results

The COPD group had a higher frequency of apoptotic cells compared to TB and LC group. The TB group showed a higher frequency of DNA damage, defect in cytokinesis, apoptotic and necrotic cells. Patients with LC had low frequency of chromosomal aberrations than TB and COPD patients.

Conclusion

COPD patients showed cellular abnormalities that corresponded to cell death by apoptosis and necrosis, while patients with TB presented defects in cytokinesis and dysfunctions in DNA repair that resulted in the formation of micronucleus (MN) besides apoptotic and necrotic cells. Patients with COPD, TB and LC had a low frequency of permanent DNA damage.

Related collections

Most cited references 26

Record: found
Abstract: found
Article: found

Is Open Access

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

Athanasios Valavanidis, Thomais Vlachogianni, Konstantinos Fiotakis … (2013)

Reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress in the respiratory system increase the production of mediators of pulmonary inflammation and initiate or promote mechanisms of carcinogenesis. The lungs are exposed daily to oxidants generated either endogenously or exogenously (air pollutants, cigarette smoke, etc.). Cells in aerobic organisms are protected against oxidative damage by enzymatic and non-enzymatic antioxidant systems. Recent epidemiologic investigations have shown associations between increased incidence of respiratory diseases and lung cancer from exposure to low levels of various forms of respirable fibers and particulate matter (PM), at occupational or urban air polluting environments. Lung cancer increases substantially for tobacco smokers due to the synergistic effects in the generation of ROS, leading to oxidative stress and inflammation with high DNA damage potential. Physical and chemical characteristics of particles (size, transition metal content, speciation, stable free radicals, etc.) play an important role in oxidative stress. In turn, oxidative stress initiates the synthesis of mediators of pulmonary inflammation in lung epithelial cells and initiation of carcinogenic mechanisms. Inhalable quartz, metal powders, mineral asbestos fibers, ozone, soot from gasoline and diesel engines, tobacco smoke and PM from ambient air pollution (PM10 and PM2.5) are involved in various oxidative stress mechanisms. Pulmonary cancer initiation and promotion has been linked to a series of biochemical pathways of oxidative stress, DNA oxidative damage, macrophage stimulation, telomere shortening, modulation of gene expression and activation of transcription factors with important role in carcinogenesis. In this review we are presenting the role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis.

0 comments Cited 235 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy?

Maziar Divangahi, Heinz G. Remold, Heinz G. Remold (2010)

Virulent Mycobacterium tuberculosis inhibits apoptosis and triggers necrosis of host macrophages to evade innate immunity and delay the initiation of adaptive immunity. By contrast, attenuated M. tuberculosis induces macrophage apoptosis, an innate defence mechanism that reduces bacterial viability. In this Opinion article, we describe how virulent M. tuberculosis blocks production of the eicosanoid lipid mediator prostaglandin E(2) (PGE(2)). PGE(2) production by infected macrophages prevents mitochondrial damage and initiates plasma membrane repair, two processes that are crucial for preventing necrosis and inducing apoptosis. Thus, M. tuberculosis-mediated modulation of eicosanoid production determines the death modality of the infected macrophage, which in turn has a substantial impact on the outcome of infection.

0 comments Cited 183 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Buccal micronucleus cytome assay.

Siegfried Knasmueller, Michael Fenech, Stefano Bonassi … (2008)

The Buccal Micronucleus Cytome (BMCyt) assay is a minimally invasive method for studying DNA damage, chromosomal instability, cell death and the regenerative potential of human buccal mucosal tissue. This method is increasingly used in molecular epidemiological studies for investigating the impact of nutrition, lifestyle factors, genotoxin exposure and genotype on DNA damage, chromosome malsegregation and cell death. The biomarkers measured in this assay have been associated with increased risk of accelerated ageing, cancer and neurodegenerative diseases. This protocol describes one of the current established methods for buccal cell collection using a small-headed toothbrush, the generation of a single-cell suspension, slide preparation using cytocentrifugation, fixation and staining using Feulgen and Light Green for both bright field and fluorescence microscopic analysis. The scoring criteria for micronuclei and other nuclear anomalies are also described in detail. The protocol in its current form takes approximately 4 h to complete from the time of buccal cell collection to the generation of stained slides for microscopic analysis.

0 comments Cited 118 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Andréa Lúcia Gonçalves da Silva: (55) 021513717 7387 , andreag@unisc.br

Maribel Josimara Bresciani: maribeljbresciani@mx2.unisc.br

Thaís Evelyn Karnopp: tekarnopp@gmail.com

Augusto Ferreira Weber: augustofweber@mx2.unisc.br

Joel Henrique Ellwanger: joel.ellwanger@gmail.com

João Antonio Pêgas Henriques: pegas@cbiot.ufrgs.br

Andréia Rosane de Moura Valim: avalim@unisc.br

Lia Gonçalves Possuelo: liapossuelo@unisc.br

Journal

Journal ID (nlm-ta): Multidiscip Respir Med

Journal ID (iso-abbrev): Multidiscip Respir Med

Title: Multidisciplinary Respiratory Medicine

Publisher: BioMed Central (London )

ISSN (Print): 1828-695X

ISSN (Electronic): 2049-6958

Publication date (Electronic): 19 December 2015

Publication date PMC-release: 19 December 2015

Publication date Collection: 2015

Volume: 10

Electronic Location Identifier: 38

Affiliations

[ ]Department of Health and Physical Education, University of Santa Cruz do Sul – UNISC, Avenida Independência, 2293, Bairro Universitário, Santa Cruz do Sul, RS CEP 96815-900 Brazil

[ ]Department of Biology and Pharmacy, University of Santa Cruz do Sul - UNISC, Santa Cruz do Sul, RS Brazil

[ ]Graduate Program in Cellular and Molecular Biology, Federal University of Rio Grande do Sul - UFRGS, Porto Alegre, RS Brazil

[ ]Graduate Program in Health Promotion, University of Santa Cruz do Sul - UNISC, Santa Cruz do Sul, RS Brazil

Article

Publisher ID: 34

DOI: 10.1186/s40248-015-0034-z

PMC ID: 4684909

PubMed ID: 26688728

SO-VID: 9e70107b-7801-4bbd-b339-8a9cf3092902

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 30 September 2015

Date accepted : 18 November 2015

Funding

Funded by: FundRef , FAPERGS/MS/CNPq/SESRS;

Award ID: 1128-2551/13-7

Award Recipient : Andréa Lúcia Gonçalves da Silva

Custom metadata

ScienceOpen disciplines: Respiratory medicine

Keywords: apoptosis,micronucleus,necrosis,pulmonary diseases

Data availability:

ScienceOpen disciplines: Respiratory medicine

Keywords: apoptosis, micronucleus, necrosis, pulmonary diseases

Comments

Comment on this article

scite_

Cited by 8

See all cited by

Most referenced authors 368

See all reference authors

DNA damage and cellular abnormalities in tuberculosis, lung cancer and chronic obstructive pulmonary disease

Read this article at

Abstract

Background

Methods

Results

Conclusion

Related collections

Biomarkers for Inflammatory Lung Disease

Most cited references 26

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

Evasion of innate immunity by Mycobacterium tuberculosis: is death an exit strategy?

Buccal micronucleus cytome assay.

Author and article information

Contributors

Journal

Affiliations

Article

History

Funding

Categories

Custom metadata

Comments

Comment on this article

Similar content 152

Cited by 8

Most referenced authors 368