Changes in levels of 8-hydroxyguanine in DNA, its repair and OGG1 mRNA in rat lungs after intratracheal administration of diesel exhaust particles

Tsurudome, Yosuke; Hirano, Takeshi; Tanaka, Isamu; Sagai, Masaru; Hirano, Hideyasu; Nagata, Naoki; Itoh, Hideaki; Kasai, Hiroshi

doi:10.1093/carcin/20.8.1573

Cited by 133 publications

(68 citation statements)

References 40 publications

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“…For example, one of the environmental pollutants, diesel exhaust particles (DEP), is known to generate ROS and induce lung cancer in experimental animals. The treatment of rats with DEP resulted in dose-and time-dependent changes in the levels of 8-oxo-G as well as the induction of hOGG1 mRNA (44). In addition, the hOGG1 gene expression level was elevated after rats were exposed to crocidolite asbestos, which is associated with epithelial cell injury in the process of carcinogenesis via oxidative stress (45).…”

Section: Figmentioning

confidence: 99%

Transcription Factors NF-YA Regulate the Induction of Human OGG1 Following DNA-alkylating Agent Methylmethane Sulfonate (MMS) Treatment

Lee

Kim

Cho

et al. 2004

Journal of Biological Chemistry

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A human 8-oxoguanine-DNA glycosylase (hOGG1) is the main enzyme that repairs 8-oxoG, which is a critical mutagenic lesion. There is a great deal of interest in the up-or down-regulation of OGG1 expression after DNA damage. In this study, we investigated the effect of a DNA-alkylating agent, methylmethane sulfonate (MMS), on hOGG1 expression level and found that MMS treatment resulted in an increase in the functional hOGG1 expression in HCT116 cells. A region between ؊121 and ؊61 of the hOGG1 promoter was found to be crucial for this induction by MMS. Site-directed mutations of the two inverted CCAAT motifs substantially abrogated the induction of the hOGG1 promoter as a result of MMS treatment. In addition, the NF-YA protein (binding to the inverted CCAAT box) was induced after exposing cells to MMS. Moreover, gel shift and supershift analyses with the nuclear extracts prepared from HCT116 cells identified NF-YA as the transcription factor interacting with the inverted CCAAT box. Mutations of the inverted CCAAT box either prevented the binding of this factor or abolished its activation as a result of MMS treatment. Finally, this study showed that hOGG1-expressing HCT116 cells exhibited increased hOGG1 repair activity and resistance to MMS. Overall, these results demonstrate that MMS can up-regulate hOGG1 expression through the induction of the transcription factor, NF-YA, and increased transcription level of the hOGG1 gene correlates with an increase in enzyme activity providing functional protection from MMS.Reactive oxygen species (ROS) 1 causes a variety of damage to DNA, including oxidized bases, abasic (AP) sites, strand breaks, and DNA-protein cross-links (1-6). Among oxidative lesions, 8-oxoguanine (8-oxoG) is one of the major base lesions formed after oxidative attack to DNA (7). Relatively large quantities of 8-oxoG are produced in mammalian cells, either as a byproduct of the normal oxidative metabolism, or as a result of exogenous sources of ROS, such as ionizing radiation, single oxygen sensitizer dyes, and redox-active organic molecules (8). 8-oxoG preferentially mispairs with adenosine during replication and thereby gives rise to G:C 3 T:A transversion mutations (9 -12). Because of its persistent generation, relative abundance, and potent mutagenicity, 8-oxoG is believed to represent a major source of spontaneous mutagenesis in all aerobic cells. In order to prevent the mutagenic effect of 8-oxoG, the bacterium, Escherichia coli, contains a GO system (13-15). The bacteria GO system consists of three proteins: MutM (also known as the Fpg protein), a DNA glycosylase/lyase that recognizes 8-oxoG:C and catalyzes the excision of 8-oxoG (16, 17); MutY, which is a DNA glycosylase that recognizes 8-oxoG:A and catalyzes the excision of A (18); and MutT, specific phosphatase that cleaves 8-oxo-dGTP (19). In mammalian cells, the main defense enzyme against the mutagenic effects of 8-oxoG in cellular DNA is 8-oxoguanine-DNA glycosylase (OGG1), which is structurally unrelated but functionally similar to formami...

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Section: Figmentioning

confidence: 99%

Transcription Factors NF-YA Regulate the Induction of Human OGG1 Following DNA-alkylating Agent Methylmethane Sulfonate (MMS) Treatment

Lee

Kim

Cho

et al. 2004

Journal of Biological Chemistry

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“…[23][24][25][26][27][28][29] Recently, it was demonstrated that 8-oxoguanine-DNA glycosylase gene (OGG1) mRNA is a useful marker of cellular oxidative stress during carcinogenesis, in addition to levels of 8-OHdG in DNA and its repair. 30 CYP3A2 expression, induced by PB, ␣-BHC, DDT and so on, is regulated by several factors. For example, Carlson et al 31 reported Interleukin-1␤ (IL-1␤) and tumor necrosis factor-␣ (TNF-␣) decrease the level of CYP3A2 and the downregulation of CYP3A2 is directly associated with NO production.…”

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confidence: 99%

Detailed low‐dose study of 1,1‐b™IS(p‐chlorophenyl)‐2,2,2‐ trichloroethane carcinogenesis suggests the possibility of a hormetic effect

Sukata

Uwagawa

Ozaki

et al. 2002

Intl Journal of Cancer

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To obtain information on the effects of nongenotoxic carcinogens at low doses for human cancer risk assessment, the carcinogenic potential of the organochlorine insecticide, 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), in the liver was assessed in F344 rats. In experiment 1, 240 male animals, 21 days old, were administered 0, 0.5, 1.0, 2.0, 5.0, 20, 100 and 500 ppm DDT in the diet for 16 weeks. Experiment 2 was conducted to elucidate the carcinogenic potential of DDT at lower levels using 180 rats given doses of 0, 0.005, 0.01, 0.1, 0.2 and 0.5 ppm. The livers of all animals were immunohistochemically examined for expression of glutathione S-transferase placental form (GST-P), putative preneoplastic lesions. Quantitative values for GST-P-positive foci in the liver were increased dose-dependently in rats given 20 ppm DDT and above with statistical significance as compared with the concurrent control value. In contrast, doses of 0.005 and 0.01 ppm were associated with a tendency for decrease below the control value, although not significantly. Western blotting analysis show that cytochrome P-450 3A2 (CYP3A2) protein expression tended to decrease at 0.005 and 0.01 ppm, a good correlation being observed with the change in the number of GST-P-positive foci. These findings suggest that a DDT hepatocarcinogenicity may show nonlinear response, that is, hormetic response at low doses. Furthermore, since CYP3A2 protein expression appears to be important for the effects of phenobarbital and the ␣-isomer of benzene hexachloride, mRNAs for IL-1 receptor type 1 (IL-1R1) and TNF-␣ receptor type 1 (TNFR1) whose ligands have roles not only in downregulating CYP3A2 expression but also in inducing antiproliferative effect or apoptosis in hepatocyte were examined. Increase was observed at low doses of DDT. Oxidative stress in liver DNA, assessed in terms of 8-hydroxydeoxyguanosine as a marker, was also decreased. These findings suggest that the possible hormetic effect that was observed in our detailed low-dose study of DDT carcinogenesis, although not statistically significant, may be linked to levels of oxidative stress and proinflammatory cytokines.

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“…We and other groups have reported that some carcinogenic agents, such as cadmium compounds and diesel exhaust particles, disturbed 8-OH-Gua repair, leading to the subsequent accumulation of 8-OH-Gua (16,17,20). As for arsenic compounds, we also previously reported that sodium arsenite decreased the 8-OHGua base excision repair activity and increased the 8-OH-Gua level in the DNA of culture cells (6).…”

Section: Discussionmentioning

confidence: 71%

Fragmentation of the DNA Repair Enzyme, OGG1, in Mouse Nonparenchymal Liver Cells by Arsenic Compounds

Hirano

Kawai

Ootsuyama

et al. 2006

Genes and Environment

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Our previous work demonstrated that arsenic compounds increased 8-hydroxyguanine (8-OH-Gua) in the DNA of cultured human cells (A549) and reduced the endonuclease nicking activity for 8-OH-Gua, suggesting that arsenic compound-induced carcinogenesis was the consequence of the inhibition of DNA repair. However, the exact mechanism by which the repair systems were disturbed was unknown. To elucidate the mechanism, we analyzed mouse 8-oxoguanine DNA glycosylase 1 (mOGG1) expression in mouse nonparenchymal liver cells, NCTC, treated with arsenic compounds (arsenic trioxide, sodium arsenite, and sodium hydrogen arsenate). We detected a cleaved form of mOGG1 (35 kDa) in addition to normal mOGG1 (type 1a, 38 kDa) in NCTC treated with arsenic compounds. These results are similar to our previous results which showed that fragmentation of mOGG1 by etoposide was related to caspase-dependent apoptosis, and was accompanied by increased 8-OH-Gua accumulation. Taken together, our results suggested that arsenic compounds might increase 8-OH-Gua accumulation by inhibiting 8-OH-Gua repair, due to mOGG1 cleavage.

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Changes in levels of 8-hydroxyguanine in DNA, its repair and OGG1 mRNA in rat lungs after intratracheal administration of diesel exhaust particles

Cited by 133 publications

References 40 publications

Transcription Factors NF-YA Regulate the Induction of Human OGG1 Following DNA-alkylating Agent Methylmethane Sulfonate (MMS) Treatment

Transcription Factors NF-YA Regulate the Induction of Human OGG1 Following DNA-alkylating Agent Methylmethane Sulfonate (MMS) Treatment

Detailed low‐dose study of 1,1‐b™IS(p‐chlorophenyl)‐2,2,2‐ trichloroethane carcinogenesis suggests the possibility of a hormetic effect

Fragmentation of the DNA Repair Enzyme, OGG1, in Mouse Nonparenchymal Liver Cells by Arsenic Compounds

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