Changes of 8-OH-dG levels in DNA and its base excision repair activity in rat lungs after inhalation exposure to hexavalent chromium

Maeng, Seung-Hee; Chung, Hai Won; Yu, Il-Je; Kim, Hyeon-Yeong; Lim, Changjin; Kim, Kwang-Jong; Kim, Soojin; Ootsuyama, Yuko; Kasai, Hiroshi

doi:10.1016/s1383-5718(03)00154-2

Cited by 36 publications

(21 citation statements)

References 28 publications

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“…Chromium also inhibits DNA repair activity. Maeng et al showed that 8‐hydroxydeoxyguanine repair enzyme activity decreases in the lung tissues of rats with chromate inhalation [32]. Hodges et al reported that the DNA‐repair endonuclease 8‐oxo‐guanine DNA glycosylase 1 is downregulated by sodium dichromate in the human lung cancer cell line, A549 [33].…”

Section: Discussionmentioning

confidence: 99%

Microsatellite instability and protein expression of the DNA mismatch repair gene,hMLH1, of lung cancer in chromate-exposed workers

et al. 2005

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Our previous studies of lung cancer in chromate-exposed workers (chromate lung cancer) have revealed that the frequency of replication error (RER) in chromate lung cancer is very high. We examined whether the RER phenotype of chromate lung cancer is due to an abnormality of DNA mismatch repair protein. We investigated the expression of a DNA mismatch repair gene, hMLH1, and hMSH2 proteins using immunohistochemistry and microsatellite instability (MSI) in 35 chromate lung cancers and 26 nonchromate lung cancers. Lung cancer without MSI or with MSI at one locus was defined as "RER(-)," lung cancer with MSI at two loci was defined as "RER(+)," and lung cancer with MSI at three or more loci was defined as "RER(++)." The repression rate of hMLH1 and hMSH2 proteins in chromate lung cancer was significantly more than that of nonchromate lung cancer (hMLH1: 56% vs. 20%, P = 0.006, hMSH2: 74% vs. 23%, P < 0.0001). In chromate lung cancer, the repression rate for hMLH1 was 43% in RER(-), 40% in RER(+), and 90% in the RER(++) group. The repression rate of hMLH1 protein in the RER(++) group was significantly higher than that in the RER(-) and RER(+) groups (P = 0.039). The inactivation of hMLH1 expression strongly correlated with the microsatellite high instability phenotype in chromate lung cancer. The genetic instability of chromate lung cancer is due to the repression of hMLH1 protein.

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Section: Discussionmentioning

confidence: 99%

Microsatellite instability and protein expression of the DNA mismatch repair gene,hMLH1, of lung cancer in chromate-exposed workers

et al. 2005

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“…OGG1 , the glycosylase that repairs 8-oxo-guanine, was down-regulated by sodium dichromate in A549 cells (human lung cancer cells) (Hodges and Chipman, 2002). Rats exposed to chromate by inhalation contained lung tissue that displayed decreased expression of OGG1 (Maeng et al, 2003). By inhibiting OGG1 , ROS-induced damage generated by Cr (VI) goes unrepaired.…”

Section: Dna Methylation and Metal-induced Carcinogenesismentioning

confidence: 99%

Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis

Brocato

Costa

2013

Critical Reviews in Toxicology

129

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DNA methylation plays an intricate role in the regulation of gene expression and events that compromise the integrity of the methylome may potentially contribute to disease development. DNA methylation is a reversible and regulatory modification that elicits a cascade of events leading to chromatin condensation and gene silencing. In general, normal cells are characterized by gene-specific hypomethylation and global hypermethylation, while cancer cells portray a reverse profile to this norm. The unique methylome displayed in cancer cells is induced after exposure to carcinogenic metals such as nickel, arsenic, cadmium, and chromium (VI). These metals alter the DNA methylation profile by provoking both hyper- and hypomethylation events. The metal-stimulated deviations to the methylome are possible mechanisms for metal-induced carcinogenesis and may provide potential biomarkers for cancer detection. Development of therapies based on the cancer methylome requires further research including human studies that supply results with larger impact and higher human relevance.

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“…According to previous studies, Cr-induced genomic DNA damage includes 8-hydroxydeoxyguanosine (8-OH-dG, 7,8-dihydro-8-oxodeoxyguanosine), which is a form of oxidative DNA damage [16]. Maeng et al [17] observed changes in 8-OH-dG levels in DNA when rats were exposed to Cr (VI) and suggest that DNA damage caused by Cr (VI) compounds may be partially associated with oxidative stress. Cr (VI) generates reactive oxygen species (ROS) and free radicals (FRs) via its intracellular reduction to Cr (III) via the Fenton and Haber-Weiss reaction [15, 18, 19].…”

Section: Introductionmentioning

confidence: 99%

Antigenotoxic and Apoptotic Activity of Green Tea Polyphenol Extracts on Hexavalent Chromium-Induced DNA Damage in Peripheral Blood of CD-1 Mice: Analysis with Differential Acridine Orange/Ethidium Bromide Staining

Garcia‐Rodriguez

Carvente-Juárez

Altamirano-Lozano

2013

Oxidative Medicine and Cellular Longevity

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This study was conducted to investigate the modulating effects of green tea polyphenols on genotoxic damage and apoptotic activity induced by hexavalent chromium [Cr (VI)] in CD-1 mice. Animals were divided into the following groups: (i) injected with vehicle; (ii) treated with green tea polyphenols (30 mg/kg) via gavage; (iii) injected with CrO3 (20 mg/kg) intraperitoneally; (iv) treated with green tea polyphenols in addition to CrO3. Genotoxic damage was evaluated by examining micronucleated polychromatic erythrocytes (MN-PCEs) obtained from peripheral blood at 0, 24, 48, and 72 h after treatment. Induction of apoptosis and cell viability were assessed by differential acridine orange/ethidium bromide (AO/EB) staining. Treatment of green tea polyphenols led to no significant changes in the MN-PCEs. However, CrO3 treatment significantly increased MN-PCEs at 24 and 48 h after injection. Green tea polyphenols treatment prior to CrO3 injection led to a decrease in MN-PCEs compared to the group treated with CrO3 only. The average of apoptotic cells was increased at 48 h after treatment compared to control mice, suggesting that apoptosis could contribute to eliminate the DNA damaged cells induced by Cr (VI). Our findings support the proposed protective effects of green tea polyphenols against the genotoxic damage induced by Cr (VI).

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Changes of 8-OH-dG levels in DNA and its base excision repair activity in rat lungs after inhalation exposure to hexavalent chromium

Cited by 36 publications

References 28 publications

Microsatellite instability and protein expression of the DNA mismatch repair gene,hMLH1, of lung cancer in chromate-exposed workers

Microsatellite instability and protein expression of the DNA mismatch repair gene,hMLH1, of lung cancer in chromate-exposed workers

Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis

Antigenotoxic and Apoptotic Activity of Green Tea Polyphenol Extracts on Hexavalent Chromium-Induced DNA Damage in Peripheral Blood of CD-1 Mice: Analysis with Differential Acridine Orange/Ethidium Bromide Staining

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