Induction of deoxyribonucleic acid degradation inEscherichia coli by ozone

Hamelin, Claude; Sarhan, Fathey; Chung, Young Sup

doi:10.1007/bf02034684

Cited by 29 publications

(20 citation statements)

References 9 publications

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“…Free radicals can cause damage to DNA, possibly by a scission of the sugar-phosphate backbone, producing strand breaks (Lesko et al, 1980;Brown & Fridovich, 1981;Simic & Jovanovic, 1986). Thus, 0, has, been shown to cause DNA single-strand breaks and/or doublestrand breaks in L929 fibroblasts (Ven der Zee et al, 1987a), wildtype Escherichia coli (Hamelin et al, 1978), calf thymus DNA (Ven Der Zee et al, 1987b), and alveolar macrophages (B,ermljdez et al 1991). Chromosome aberration and/or sister chromatid exchanges have been observed after an in vivo 0, exposure in the peripheral lymphocytes of animals (Zelac et al, 1971;Mckenzie et al, 1977) and humans (Merz et al, 1975;Guerrero et al, 1979).…”

mentioning

confidence: 95%

Ozone-Induced Dna Strand Breaks in Guinea Pig Tracheobronchial Epithelial Cells

Ferng

Castro

Afifi

et al. 1997

Journal of Toxicology and Environmental Health

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Ozone (O,), the major oxidant of photochemical smog, is thought to be genotoxic and a potential respiratory carcinogen or promoter of carcinogenic processes. Because of oxidative reactions with the mucus in the upper airway, 0, reaction products are able to penetrate into the tracheobronchial epithelial (TE) cells. The carcinogenic effects of 0, on the TE cells are especially of interest since most previous studies have focused on the morphology or permeability changes of tracheas only. Therefore, the objective of this study was to examine the potential 0, genotoxicity in TE cells after an in vivo exposure, using DNA strand breaks as an index. Two-month-old male Dunkin-Hartley guinea pigs, specific pathogen free, 4 in each group, were exposed to 1.0 ppm 0, for 0, 12, 24, 48, 72, or 96 h. Animals exposed to filtered air without 0, exposure were used as controls. After 0, exposure, the trachea with two main bronchi was removed from each animal, and TE cells were isolated and employed for determination of DNA strand breaks by fluorometric analysis of DNA unwinding (FADU). The statistical significance level was set at a = .05. Compared with controls, ozone exposure did not alter the TE cell yield or viability, but caused an increase in protein content in tracheal lavage and an increase in DNA strand breaks. The amount of DNA left in the alkali lysate of TE cells found at 72 h exposure was significantly decreased from controls for 3 different alkali incubation times. An increase of the double-stranded DNA left in the alkali lysate of TE cells was observed at 96 h of exposure and approached the value of 24 h of exposure. The same pattern was seen with all 3 different alkali incubation times at lS°C. One Q, unit was estimated to correspond to 100 strand breaks per cell. The Q, was also used as an indicator for 0, damage. Compared to controls, the Q, increases significantly after I ppm 0, exposure for 72 h, regardless of the alkali incubation time at 15°C.

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mentioning

confidence: 95%

Ozone-Induced Dna Strand Breaks in Guinea Pig Tracheobronchial Epithelial Cells

Ferng

Castro

Afifi

et al. 1997

Journal of Toxicology and Environmental Health

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“…DNA damage stimulates polyADP-ribosylatio n as an apparent requirement for DNA repair (Shall, 1984(Shall, , 1994Satoh & Lindahl, 1992;Malanga & Althaus, 1994), since the inhibitor of polyADPR synthetase greatly retards the DNA repair process (Cristóvâo & Rueff, 1996;Ménissier de Murcia et al, 1997;Trucco et al, 1998;Masutani et al, 1999). 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.…”

Section: Discussionmentioning

confidence: 90%

“…Also, in vivo exposure to NO 2 can induce mutations and chromosome aberrations in rat lung cells (Isomura et al, 1984). Exposure to O 3 has been shown to cause DNA single-strand breaks and double-strand breaks (Hamelin et al, 1978;Van der Zee et al, 1987a, 1987b. In vivo exposure to ozone increases DNA single-strand breaks in human and guinea pig lung cells (Lee et al, 1995).…”

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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“…However, as the counts decreased (higher oxidant doses or longer contact times) a marked difference was observed between the metabolic activities after the two treatments: at the same microbial counts, the chlorine-treated culture exhibits higher respiratory activity (OUR and DHA a ) than that observed after applying ozone; therefore, ozone antimicrobial action was stronger. With regard to this, different studies on inactivation of E. coli with ozone indicated that lysis of the cells can result for high concentrations or extended ozone contact times (Perrich et al, 1975;Hamelin et al, 1978). Hunt and Mariñas (1999) indicated that noticeable changes in the interior of E. coli cells did not take place until most of the cells were non-viable, while subsequent exposure to ozone resulted in structural changes, membrane deterioration, and ultimately lysis of the inactivated cells.…”

Section: Analysis Of the Effect Of Ozone On Biomass Concentration In mentioning

confidence: 99%

“…Ishizaki et al (1987) suggested that ozone was able to diffuse through the cell membrane and react with bio-molecules and indicated that damage to chromosomal DNA might be one of the reasons for inactivation of E. coli. Other authors working with E. coli indicated that lysis of the inactivated cells can result after prolonged ozonation (Perrich et al, 1975;Hamelin et al, 1978;Hunt and Mariñas, 1999). White (1999) indicated that ozone disinfection is a direct result of cell wall disintegration and cell lysis.…”

Section: Introductionmentioning

confidence: 99%

Effectiveness of chlorination and ozonation methods on pure cultures of floc-forming micro-organisms and activated sludge: A comparative study

Caravelli¹,

Giannuzzi²,

Zaritzky³

2007

WSA

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Chlorination is a very useful control method of filamentous bulking in activated sludge systems; however, it favours formation of undesirable compounds such as trihalomethanes. Other oxidants, such as ozone, could be used for bulking control. In view of the fact that chlorine and ozone are both non-selective chemical agents affecting filamentous and floc-forming micro-organisms, the determination of optimum dosage conditions becomes essential to minimise the impact produced on the activated sludge process. In this work, the effects of chlorine and ozone on the biomass concentration of activated sludge and on different parameters that characterise the microbial metabolic activity were compared. The following techniques were applied: Respirometry (oxygen uptake rate); and INT-dehydrogenase activity test carried out both by spectrophotometry (DHA a ) and image analysis (DHA i ). The respirometric technique and the DHA a test quantified oxidants action on the total respiratory activity of flocs; the image DHA i test was applied to evaluate the specific action of the oxidants on filamentous micro-organisms. Additionally, plate count technique, respirometry and DHA a test were correlated using chlorine and ozone experiments on pure cultures of a floc-forming micro-organism (Acinetobacter anitratus) to compare the effect of the oxidising agents on the metabolic activity and the viability of the micro-organisms. Ozone was found to have more intense antimicrobial action. In activated sludge, ozone reduced total biomass concentration by oxidising various components and causing cell lysis. An equation was proposed to estimate biomass concentration of activated sludge as a function of time and ozone dose rate; in contrast, at the doses applied, chlorine did not reduce the concentration of activated sludge biomass. In activated sludge, adequate conditions for both oxidants were identified under which the respiratory activity of filamentous micro-organisms could be considerably inhibited, causing the lowest possible impact on whole floc metabolic activity. An initial chlorine dose of 7.9 mgCl 2 ·gVSS -1 for a contact time of 5 min (initial pulse= 6.0 mgCl 2 ·ℓ -1 ), and a total ozone dose of 66.0 mgO 3 ·gVSS -1 (ozone dose rate of 3.3 mgO 3 ·gVSS -1 ·min -1 for a contact time of 20 min) were the most suitable conditions to control filamentous bulking.

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Induction of deoxyribonucleic acid degradation inEscherichia coli by ozone

Cited by 29 publications

References 9 publications

Ozone-Induced Dna Strand Breaks in Guinea Pig Tracheobronchial Epithelial Cells

Ozone-Induced Dna Strand Breaks in Guinea Pig Tracheobronchial Epithelial Cells

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

Effectiveness of chlorination and ozonation methods on pure cultures of floc-forming micro-organisms and activated sludge: A comparative study

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