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

Abstract

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.

Association between atmospheric ozone levels and damage to human nasal mucosa in Florence, Italy

“…More recently it has been shown that ozone is capable of inducing DNA strand breaks upon in vitro exposure of cells of the respiratory tract [Lee et al, 1996;Ferng et al, 1997] and human leukocytes, via hydrogen peroxide formation [Diaz-Llera et al, 2002]. This paper is the first report of an association between ozone concentration in urban air and DNA damage in the nasal mucosa of humans.…”

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

“…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.…”

“…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.…”

Bacillus subtilis devitalization mechanism of atmosphere pressure plasma jet

“…This etching action eroded cell materials, as a result, cell membrane ruptured and the content effused, and caused cell to die finally [18]. In addition, the chemical reactive species also reacted with the cell materials at the same time.…”