Measurement of oxidative DNA damage induced by mainstream cigarette smoke in cultured NCI-H292 human pulmonary carcinoma cells

Thorne, David; Wilson, James B.; Kumaravel, T. S.; Massey, Eian D.; McEwan, Michael

doi:10.1016/j.mrgentox.2008.11.008

Cited by 56 publications

(53 citation statements)

References 25 publications

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“…Moreover, using the comet assay combined with endonuclease treatment, which detects the formation of 8-oxodeoxyguanosine (8-oxodG), a critical biomarker of oxidative damage to DNA (14), Thorne and colleagues observed that the damage was induced in DNA following exposure of human pulmonary cancer cells to mainstream cigarette smoke (15). In contrast, no increase in 8-oxodG levels was found following ECS exposure of larval Drosophila in our recent study.…”

Section: Introductionmentioning

confidence: 73%

Exposure to Cigarette Smoke Increases Urate Level and Decreases Glutathione Level in Larval Drosophila melanogaster

Fujiwara

Hamatake

Arimoto

et al. 2011

Genes and Environment

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Recently, we reported experimental evidence to support the notion that in Drosophila melanogaster, urate is involved in defense against toxic eŠects of environmental cigarette smoke (ECS). To obtain further information pertaining to the defense mechanisms involving urate and other antioxidants, the present study measured the levels of urate, its precursors and glutathione, and SOD activity in larval ‰ies of wild-type strains (Oregon-R and Canton-S) and two urate-null mutant strains (ma-l and ry 1 ) following exposure to ECS for various durations. In both wild type strains, unlike the case in either of the mutant strains, the urate level signiˆcantly increased above the basal level in a manner dependent on the duration of ECS exposure. Similar increases in the level of urate precursors were found in Canton-S and in both of the urate-null strains. There was a slight increase in glutathione level above the control level following ECS exposure for a short time, followed by an exposure-dependent decrease to less than 60% of the control level within the exposure range used in all of the four strains. On the other hand, no appreciable change was found in the SOD activity prior to or following ECS exposure, irrespective of the strain examined. In terms of the survival of treated larvae to adulthood under the conditions used for the measurements of urate and others, it was found that wild-type strain Canton-S was as sensitive as the urate-null mutant strains and clearly more sensitive than wild-type strains Oregon-R and Hikone-R. This was so despite the fact that, compared with Oregon-R, Canton-S contained urate at relatively higher levels prior to and following ECS exposure, and that the glutathione levels in Canton-S prior to and following treatment were comparable with those in other strains. These results are discussed with respect to the involvement of urate and glutathione in defense against the toxicity of ECS and the possible existence of another defense mechanism which is deˆcient in the Canton-S strain.

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Section: Introductionmentioning

confidence: 73%

Exposure to Cigarette Smoke Increases Urate Level and Decreases Glutathione Level in Larval Drosophila melanogaster

Fujiwara

Hamatake

Arimoto

et al. 2011

Genes and Environment

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“…2A), suggesting that arsanilic acid induces DNA damage in Sertoli cells. The rate of DNA tail was used to show the degree of DNA damage which was classified into grades 0 to 4 [2,21]. Table 3 shows that the degree of DNA damage in the control group did not reach grades 3 and 4 and that 91.56% of DNA damage was classified into grade 0.…”

Section: Dna Damage Of Piglet Sertoli Cells Caused By Arsanilic Acidmentioning

confidence: 99%

DNA Damage and Decrease of Cellular Oxidase Activity in Piglet Sertoli Cells Exposed to Arsanilic Acid

Zhang

Yuan

et al. 2011

The Journal of Veterinary Medical Science

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ABSTRACT. The study was designed to explore the toxic effects of arsanilic acid on piglet Sertoli cells. Sertoli cells were isolated from piglet testes using a two-step enzyme digestion followed by differential plating. Piglet Sertoli cells were cultured and classified into the following five groups: group A, the control without arsanilic acid treatment; group B, cultured with 5 µM arsanilic acid; group C, cultured with 50 µM arsanilic acid; group D, cultured with 0.5 mM arsanilic acid; and group E, cultured with 5 mM arsanilic acid. We found that Sertoli cell growth was inhibited by arsanilic acid at 0.5 mM compared with the control, group A. The oxidase activity of Sertoli cells was decreased by arsanilic acid at 0.5 mM as evidenced by the observations that arsanilic acid increased MDA content but decreased the SOD and GSH-Px activities of Sertoli cells. Moreover, 50 µM of arsanilic acid was observed to cause DNA damage in Sertoli cells. The results of our study suggest that exposure of Sertoli cells to arsanilic acid leads to induction of oxidative stress and inhibition of cell growth at a high concentration, while arsanilic acid causes DNA damage in Sertoli cells at a low concentration.

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“…[1,2] Indeed, hastening oxidative processes can lead to an altered intracellular redox status causing cellular dysfunction or death [1,2] and related events, most prominently oxidative DNA damage, [3][4][5][6] a primary process of carcinogenesis. It comes as no surprise that the development of pathogenic oxidative processes in human organism is lifestyle dependent.…”

Section: Introductionmentioning

confidence: 99%

“…[2] Thus, cigarette smoking, which is considered in the literature as a risk factor for various pathological developments and diseases (such as chronic bronchitis, emphysema, cardiovascular disease, carcinogenic developments, and tumour growth [7][8][9][10][11][12][13][14] ) causes, in particular, the oxidative damage of cell membranes and biological macromolecules. [6,[15][16][17][18][19][20][21][22][23] Cigarette smoke is a complex chemical conglomerate that contains high concentrations of two distinctly different fractions of free radicals, one in its gas phase (GP) and another one in the particulate matter (tar). [16,17,[24][25][26][27] The GP of the smoke predominantly contains reactive carbon-and oxygencentred radicals, as well as a rather sizable amount of nitric oxide.…”

Section: Introductionmentioning

confidence: 99%

Effects of Different Phases of Cigarette Smoke on Lipid Peroxidation and Membrane Structure in Liposomes

et al. 2014

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This paper discloses for the first time the effects of the gas phase (GP) and the tar of cigarette smoke on lipid peroxidation (LPO) and on the structure of different lipid regions in liposomes. The LPO development was analysed in terms of the total unsaturation of lipids (double-bond, DB, content) and the formation of dienic conjugates (DC), ketodienes (KD), and malonic dialdehyde (MDA). As expected, the exposure of liposomes to either the GP or the tar led to a significant decrease in the DB content. However, the formation of oxidation products revealed different dynamics: MDA generation was inhibited, while the formation of DC and KD increased during the first few hours of the LPO development followed by its inhibition. The smoke constituents exhibited opposite effects on the structure of the lipid bilayer of liposomes: the GP markedly enhanced the microviscosity of liposomal membranes, whereas the tar caused a drastic lowering of microviscosity.

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Measurement of oxidative DNA damage induced by mainstream cigarette smoke in cultured NCI-H292 human pulmonary carcinoma cells

Cited by 56 publications

References 25 publications

Exposure to Cigarette Smoke Increases Urate Level and Decreases Glutathione Level in Larval Drosophila melanogaster

Exposure to Cigarette Smoke Increases Urate Level and Decreases Glutathione Level in Larval Drosophila melanogaster

DNA Damage and Decrease of Cellular Oxidase Activity in Piglet Sertoli Cells Exposed to Arsanilic Acid

Effects of Different Phases of Cigarette Smoke on Lipid Peroxidation and Membrane Structure in Liposomes

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