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

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 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.

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Assessment of Genotoxic Damage in Nurses Occupationally Exposed to Anaesthetic Gases or Antineoplastic Drugs by the Comet Assay

Journal of Occupational Health ◽

10.1539/joh.m8012 ◽

2009 ◽

Vol 51 (3) ◽

pp. 283-286 ◽

Cited By ~ 15

Author(s):

Seval Izdes ◽

Semra Sardas ◽

Ela Kadioglu ◽

Cetin Kaymak ◽

Eren Ozcagli

Keyword(s):

Comet Assay ◽

Antineoplastic Drugs ◽

Genotoxic Damage ◽

Anaesthetic Gases ◽

Occupationally Exposed

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Evaluation of immunological, inflammatory, and oxidative stress biomarkers in gasoline station attendants

BMC Pharmacology and Toxicology ◽

10.1186/s40360-019-0355-1 ◽

2019 ◽

Vol 20 (S1) ◽

Cited By ~ 2

Author(s):

Angela Maria Moro ◽

Elisa Sauer ◽

Natália Brucker ◽

Mariele Feiffer Charão ◽

Bruna Gauer ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Cytokines ◽

Linear Regression Analysis ◽

Exposed Group ◽

Oxidative Stress Biomarkers ◽

Gasoline Station ◽

Stress Biomarkers ◽

And Oxidative Stress ◽

Gst Activity ◽

Pro Inflammatory Cytokines

Abstract Background Gasoline is a complex mixture of saturated and unsaturated hydrocarbons, in which aromatic compounds, such as BTX (benzene, toluene, and xylene) feature as the main constituents. Simultaneous exposure to these aromatic hydrocarbons causes a significant impact on benzene toxicity. In order to detect early alterations caused in gasoline station attendants exposed to BTX compounds, immunological, inflammatory, and oxidative stress biomarkers were evaluated. Methods A total of 66 male subjects participated in this study. The gasoline station attendants (GSA) group consisted of 38 gasoline station attendants from Rio Grande do Sul, Brazil. The non-exposed group consisted of 28 subjects who were non-smokers and who had no history of occupational exposure. Environmental and biological monitoring of BTX exposure was performed using blood and urine. Results The GSA group showed increased BTX concentrations in relation to the non-exposed group (p < 0.001). The GSA group showed elevated protein carbonyl (PCO) levels and pro-inflammatory cytokines, decreased expression of CD80 and CD86 in monocytes, and reduced glutathione S-transferase (GST) activity compared to the non-exposed group (p < 0.05). BTX levels and trans,trans-muconic acid levels were positively correlated with pro-inflammatory cytokines and negatively correlated with interleukin-10 contents (p < 0.001). Increased levels of pro-inflammatory cytokines were accompanied by increased PCO contents and decreased GST activity (p < 0.001). Furthermore, according to the multiple linear regression analysis, benzene exposure was the only factor that significantly contributed to the increased pro-inflammatory cytokines (p < 0.05). Conclusions Taken together, these findings show the influence of exposure to BTX compounds, especially benzene, on the immunological, inflammatory, and oxidative stress biomarkers evaluated. Furthermore, the data suggest the relationship among the evaluated biomarkers of effect, which could contribute to providing early signs of damage to biomolecules in subjects occupationally exposed to BTX compounds.

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Attenuation of Doxorubicin Induced Genotoxicity in HepG2 Cells: Effect of Melatonin Loading Chitosan-Tripolyphosphate Nanoparticles on Oxidative stress

International Journal of Cancer Research & Therapy ◽

10.33140/ijcrt.05.02.01 ◽

2020 ◽

Vol 5 (2) ◽

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Comet Assay ◽

Hepg2 Cells ◽

Reactive Oxygen Species Generation ◽

Reactive Oxygen ◽

Intracellular Reactive Oxygen Species ◽

Oxygen Species ◽

Genotoxic Effects ◽

In Vivo Models

Doxorubicin is a chemotherapy medication applied in the treatment of numerous cancers. Like other topoisomerase II inhibitors, doxorubicin has been shown genotoxic effects in both in vitro and in vivo models. Melatonin acts as a potent antioxidant. In additional, anti-inflammatory, anti-apoptotic, cytoprotective and genoprotective effects of melatonin have been reported in previous studies. The aim of present study was to determine protective role of melatonin nanoparticles against doxorubicin induced-genotoxicity. HepG2 cells were treated with various concentrations of doxorubicin, melatonin and nano melatonin in both pre- and cotreatment conditions and then analyzed via comet assay. Besides the intracellular reactive oxygen species and glutathione levels have been assessed. The results of current study show that doxorubicin induced a clear genotoxic effect in HepG2 cells. Melatonin and its nanoparticles decreased the genotoxic effects of doxorubicin significantly in both types of experiment states that exhibited by comet assay. Furthermore, both forms of melatonin decreased the intracellular reactive oxygen species generation and increased the intracellular glutathione contents in HepG2 cells. However, nano melatonin was more effective in attenuating of oxidative stress and DNA damage induced by doxorubicin.

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Decreased paraoxonase 1 activity and increased oxidative stress in low lead−exposed workers

Human & Experimental Toxicology ◽

10.1177/0960327110388536 ◽

2011 ◽

Vol 30 (9) ◽

pp. 1196-1203 ◽

Cited By ~ 13

Author(s):

Thinnakorn Permpongpaiboon ◽

Amar Nagila ◽

Phannee Pidetcha ◽

Kulwadee Tuangmungsakulchai ◽

Soontharee Tantrarongroj ◽

...

Keyword(s):

Oxidative Stress ◽

Lead Exposure ◽

Linear Regression Analysis ◽

Exposed Group ◽

Paraoxonase 1 ◽

Pon1 Activity ◽

Control Group ◽

Oxidative Stress Parameters ◽

Exposed Workers ◽

Stress Parameters

Paraoxonase 1 (PON1) has been proposed as an antioxidant enzyme. Although lead-inhibited PON1 activity has been demonstrated mostly based on in vitro experiments, it is uncertain whether this phenomenon is relevant in pathogenesis of lead-induced oxidative stress in the lead exposure. We examined associations of blood lead levels (BLL) and PON1 activity along with oxidative stress parameters in lead exposure workers. We determined malondialdehyde (MDA), conjugated diene (CD), total peroxides (TP), total antioxidant status (TAS), the oxidative stress index (OSI), and PON1 activity in earthenware factory workers ( n = 60) and control subjects ( n = 65). The lead-exposed group significantly increased lipid peroxidation parameters and OSI compared to the control group ( p < 0.001). The lead-exposed group had significantly decreased PON1 activity and TAS levels compared to the control group ( p < 0.001). Multiple linear regression analysis revealed that BLL were significantly correlated with decreased TAS ( r = −0.496) and PON1 activity ( r = −0.434), but with increased CD ( r = 0.694), TP ( r = 0.614), MDA ( r = 0.788), and OSI ( r = 0.722). Interestingly, BLL at 10 µg/dL significantly decreased PON1 activity and increased oxidative stress parameters with insignificant changes in other biochemical and hematological parameters. Altogether, the reduction of PON1 activity may associate in an imbalance in pro-oxidants and antioxidants, leading to oxidative damage in lead-exposed workers even at low BLL.

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Genotoxic damage in workers exposed to pigment-grade titanium dioxide (TiO2) during paint production

European Journal of Public Health ◽

10.1093/eurpub/ckaa166.1370 ◽

2020 ◽

Vol 30 (Supplement_5) ◽

Author(s):

S a Bonetta ◽

M Macrì ◽

M Acito ◽

S i Bonetta ◽

G Castrignanò ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Titanium Dioxide ◽

Ultrafine Particles ◽

Management Practices ◽

The European Union ◽

Genotoxic Effects ◽

Early Effect ◽

Genotoxic Damage ◽

Wide Range

Abstract TiO2 is broadly used in a wide range of applications such as photocatalysis, pigments and additives. Despite the promising commercial opportunities, different studies have shown that TiO2 can induce oxidative stress, inflammatory and genotoxic effects. The European Union has classified certain titanium dioxide powders and powder mixtures containing TiO2 as a suspected carcinogen (Category 2) via inhalation. Considering that the information about the potential adverse health effects of TiO2 in occupational environment are still scarce and controversial, the purpose of the study was to investigate the genotoxic effects and oxidative stress in workers exposed to TiO2 during paint production. Biomarkers of early effect (DNA damage and micronuclei) were evaluated in the buccal cells and salivary leucocytes of 30 workers (15 production workers and 15 controls). To collect information about personal details, occupational history, medication, smoking, diet, physical activity, a questionnaire was administered to all workers. Personal and area monitoring have been carried out to determine airborne inhalable and respirable fraction of TiO2; a NanoTracer was used to monitor the presence of ultrafine particles. In spite of the low mass concentration and a mild percentage of nanoparticles, filter deposited TiO2 was in sub-micron size, thus accounting for its respirability. Preliminary results on salivary leucocytes show a slight higher DNA damage in the exposed workers as compared to the controls. Whereas biomarker assessment is still in progress, these preliminary findings show that workers are exposed to low but measurable levels of TiO2 able to induce a mild genotoxic damage. A combined approach using both personal exposure assessment and biomonitoring can improve the risk assessment in occupational settings in which TiO2 is handled. Moreover, this also suggest to take precautionary measure during specific activities and operational phases thus decreasing the risks for worker. Key messages The results of the present study may promote effective risk management practices in occupational environments that uses TiO2. The results obtained suggest the introduction of activities and operational phases with lower risks for the worker.

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Evaluation of DNA Damage and Oxidative Stress in Road Pavement Workers Occupationally Exposed to Polycyclic Aromatic Hydrocarbons

International Conference on Advances in Agricultural, Biological & Environmental Sciences (AABES-2014) Oct 15-16, 2014 Dubai (UAE) ◽

10.15242/iicbe.c1014023 ◽

2014 ◽

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Polycyclic Aromatic Hydrocarbons ◽

Aromatic Hydrocarbons ◽

Road Pavement ◽

Occupationally Exposed ◽

Polycyclic Aromatic ◽

And Oxidative Stress

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Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

Ecology and Noospherology ◽

10.15421/032001 ◽

2020 ◽

Vol 31 (1) ◽

pp. 3-10

Author(s):

V. S. Nedzvetsky ◽

V. Ya. Gasso ◽

A. M. Hahut ◽

I. A. Hasso

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Programmed Cell Death ◽

Oxidative Damage ◽

Cadmium Chloride ◽

Glioma Cells ◽

Low Doses ◽

Genotoxic Effects ◽

Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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Chemoprotective Effects of Propolis on Aflatoxin B1-Induced Hepatotoxicity in Rats: Oxidative Damage and Hepatotoxicity by Modulating TP53, Oxidative Stress

Current Proteomics ◽

10.2174/1570164617666190925121720 ◽

2020 ◽

Vol 17 (3) ◽

pp. 191-199

Author(s):

Seval Yilmaz ◽

Fatih Mehmet Kandemir ◽

Emre Kaya ◽

Mustafa Ozkaraca

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Oxidative Damage ◽

Aflatoxin B1 ◽

Tp53 Gene ◽

Control Group ◽

Glutathione S Transferase ◽

Gene Expressions ◽

Cat Gene ◽

Gst Activity

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.

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