DNA Strand Breaks Caused by Exposure to Ozone and Nitrogen Dioxide

Bermúdez, Eliezer; Sf, Ferng; Ce, Castro; Mg, Mustafa

doi:10.1006/enrs.1999.3955

Cited by 23 publications

(12 citation statements)

References 43 publications

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“…There is no simple explanation on the fact why DNA is more easily attacked by ozone than RNA, however, this result is in line with reports that ozone causes a single strand break on DNA molecules in a number of cases [21][22][23][24].…”

Section: Solid-state Ozonolysis and Ft-ir Spectroscopysupporting

confidence: 92%

DNA degradation with ozone

Cataldo¹

2006

International Journal of Biological Macromolecules

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Section: Solid-state Ozonolysis and Ft-ir Spectroscopysupporting

confidence: 92%

DNA degradation with ozone

Cataldo¹

2006

International Journal of Biological Macromolecules

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“…As mentioned in the introduction, a number of authors (Hamelin et al, 1978;Van der Zee et al, 1987a, 1987bRithidech et al, 1990;Görsdorf et al, 1990;Lee et al, 1995Lee et al, , 1996Ferng et al, 1997;Haney & Connor, 1999) have demonstrated that O 3 and NO 2 can cause DNA damage both in vitro and in vivo. In a previous publication (Bermúdez et al, 1999), we also demonstrated that ozone and nitrogen dioxide can cause DNA strand breaks in alveolar macrophages of rats exposed to similar conditions used in the present study. With this evidence, the stimulation of polyADPR synthetase observed can be attributed to DNA damage caused by exposure to NO 2 and O 3 .…”

Section: Discussionsupporting

confidence: 77%

“…Experiments (Rithidech et al, 1990) have demonstrated that in vivo exposure to ozone can cause chromosome damage in rat alveolar macrophages. More recently, other research groups have demonstrated that ozone can cause DNA strand breaks after in vivo exposure of rat tracheobronchial epithelial cells (Ferng et al, 1997), rat alveolar macrophages (Bermúdez et al, 1999), and mouse lung cells (Haney & Connor, 1999). As mentioned earlier, the ability of NO 2 and O 3 to generate free radicals suggests that damage to DNA and the subsequent DNA repair response may represent an important component of their toxicity.…”

mentioning

confidence: 97%

Detection of Poly(adp-Ribose) Synthetase Activity in Alveolar Macrophages of Rats Exposed to Nitrogen Dioxide and Ozone

Bermúdez

2001

Inhalation Toxicology

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The toxic effects of nitrogen dioxide (NO2) and ozone (O3) are mediated through the formation of free radicals, which can cause DNA strand breaks. The present study demonstrates that exposure to NO2 and O3 causes a stimulation of poly(ADP-ribose) (polyADPR) synthetase in alveolar macrophages of rats. Three-month-old male Sprague-Dawley rats, specific pathogen free, were exposed to either 1.2 ppm NO2 or 0.3 ppm O3 alone or a combination of these 2 oxidants continuously for 3 days. The control group was exposed to filtered room air. To evaluate whether exposure to these two oxidants (NO2 and O3) caused DNA damage to lung cells, the activity of polyADPR synthetase was measured. Cellular DNA repair is dependent upon the formation of poly(ADP-ribose) polymerase, which is catalyzed by polyADPR synthetase. PolyADPR synthetase is known to be activated in response of DNA damage. The results showed that the enzyme activity was stimulated after exposure to O3 or exposure to NO2 + O3. Ozone exposure caused a 25% increase in the enzyme activity as compared to the control. Combined exposure to NO2 + O3 showed a 53% increase in the enzyme activity. These results were statistically significant as compared to the control and NO(2) exposure groups. Other parameters such as total cell count, cell viability, and differential cell count were also determined. The stimulation of polyADPR synthetase activity after O3 exposure or NO2 + O3 exposure reflects a response to lung cellular DNA repair, which may be used as an indicator for assessing DNA damage caused by oxidant injury.

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“…In particular, NO 2 can induce DNA-single strand breaks in cultured animal cells and also in alveolar macrophages alone and in combination with ozone [62-64]. Particulate matter can interact with DNA either directly or after enzymatic transformation to induce DNA modifications that may be associated with increased frequencies of pollution-associated diseases, such as lung cancer [65].…”

Section: Discussionmentioning

confidence: 99%

A Review and Meta-Analysis of Outdoor Air Pollution and Risk of Childhood Leukemia

Filippini

Heck

Malagoli

et al. 2015

Journal of Environmental Science and Health, Part C

134

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Leukemia is the most frequent malignant disease affecting children. To date, the etiology of childhood leukemia remains largely unknown. Few risk factors (genetic susceptibility, infections, ionizing radiation, etc.) have been clearly identified, but they appear to explain only a small proportion of cases. Considerably more uncertain is the role of other environmental risk factors, such as indoor and outdoor air pollution. We sought to summarize and quantify the association between traffic-related air pollution and risk of childhood leukemia, and further examined results according to method of exposure assessment, study quality, leukemia subtype, time period and continent where studies took place. After a literature search yielded 6 ecologic and 20 case-control studies, we scored the studies based upon the Newcastle-Ottawa Scale. The studies assessed residential exposure to pollutants from motorized traffic by computing traffic density in the neighboring roads or vicinity to petrol stations, or by using measured or modeled nitrogen dioxide and benzene outdoor air levels. Because heterogeneity across studies was observed, random-effects summary odds ratios (OR) and 95% confidence intervals (CI) were reported. Whenever possible we additionally conducted stratified analyses comparing acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). Limiting the analysis to high-quality studies (Newcastle-Ottawa Scale ≥ 7), those using traffic density as the exposure assessment metric showed an increase in childhood leukemia risk in the highest exposure category (OR=1.07, 95% CI 0.93 – 1.24). However, we observed evidence of publication bias. Results for NO2 exposure and benzene showed an OR of 1.21 (95% CI 0.97 – 1.52) and 1.64 (95% CI 0.91 – 2.95) respectively. When stratifying by leukemia type, the results based upon NO2 were 1.21 (95% CI 1.04 – 1.41) for ALL and 1.06 (95% CI 0.51 – 2.21) for AML; based upon benzene were 1.09 (95% CI 0.67 – 1.77) for ALL and 2.28 (95% CI 1.09 – 4.75) for AML. Estimates were generally higher for exposures in the postnatal period compared to the prenatal period, and for European studies compared to North American studies. Overall, our results support a link between ambient exposure to traffic pollution and childhood leukemia risk, particularly due to benzene.

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DNA Strand Breaks Caused by Exposure to Ozone and Nitrogen Dioxide

Cited by 23 publications

References 43 publications

DNA degradation with ozone

DNA degradation with ozone

Detection of Poly(adp-Ribose) Synthetase Activity in Alveolar Macrophages of Rats Exposed to Nitrogen Dioxide and Ozone

A Review and Meta-Analysis of Outdoor Air Pollution and Risk of Childhood Leukemia

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