Effect of vitamin E on survival, glutathione reductase and formation of chromium (V) in Chinese hamster V-79 cells treated with sodium chromate (VI)

Sugiyama, Masayasu; Ando, Akikazu; Ogura, Ryohei

doi:10.1093/carcin/10.4.737

Cited by 79 publications

(61 citation statements)

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“…As a result, premutant cells are likely to be lost from the chromium-treated populations. It is also difficult to define an effective chromium treatment dosing regime, since chromium compounds are often mutagenic over a very narrow dose range (5,6,18,28). This may be partly related to residual toxicity that could result from trivalent Cr that is trapped within the cells (30).…”

Section: Resultsmentioning

confidence: 99%

Metal mutagenesis in transgenic Chinese hamster cell lines.

Klein

Kargačin

et al. 1994

Environ Health Perspect

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Metals are toxic agents for which genotoxic effects are often difficult to demonstrate. To study metal mutagenesis, we have used two stable hprt gpte transgenic cell lines that were derived from Chinese hamster V79 cells. Both the G12 and Gl0 cell lines are known to be very sensitive to clastogens such as X-rays and bleomycin, with the mutagenic response of the integrated xanthine guanine phosphoribosyl transferase (gp) gene in G10 usually exceeding that of the same gene in the transgenic G12 cells. In studies with carcinogenic insoluble nickel compounds, a high level of mutagenesis was found at the gpt locus of G12 cells but not at the endogenous hypoxanthine phosphoribosyl transferase (hpr locus of V79 cells. We have since demonstrated the similar recovery of a high frequency of viable G12 mutants with other insoluble nickel salts including nickel oxides (black and green). The relative mutant yield for the insoluble nickel compounds (G1 2>G1 0) is the opposite of that obtained with nonmetal clastogens (G10>G12). In the G12 cells, nickel mutagenesis may be related to the integration of the gpt sequence into a heterochromatic region of the genome. For some of the insoluble nickel compounds, significant inhibition of both cytotoxicity and mutant yield resulted when the G12 cells were pretreated with vitamin E. In comparison with the nickel studies, the mutagenic responses to chromium compounds in these cell lines were not as dramatic. Mutagenesis of the gpt target could not be demonstrated with other metals such as mercury or vanadium. -Environ Health Perspect 102(Suppl 3):63-67 (1994).

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Section: Resultsmentioning

confidence: 99%

Metal mutagenesis in transgenic Chinese hamster cell lines.

Klein

Kargačin

et al. 1994

Environ Health Perspect

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“…Cr(VI) is a well-established human lung carcinogen and previous studies show that Cr(VI) chromium is most potent in particulate form. Particulate Cr(VI) induces DNA strand breaks, Cr-DNA adducts, Cr-DNA crosslinks and mutation to 6-thioguanine resistance in diploid human fibroblasts [8,[14][15][16][17]12,35,36], however how these lesions are repaired and their relationship to Cr(VI)-induced CIN are uncertain.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies utilizing vitamin pretreatments have shown that adducts and crosslinks do not correlate with chromosomal aberrations [16][17][18][19]. DNA single strand breaks are very short-lived after particulate Cr(VI) exposure and thus do not seem like likely candidates for inducing chromosome damage [13].…”

Section: Introductionmentioning

confidence: 99%

Homologous recombination repair protects against particulate chromate-induced chromosome instability in Chinese hamster cells

Stackpole

Wise

Goodale

et al. 2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Particulate hexavalent chromium [Cr(VI)] compounds are well-established human carcinogens. Cr (VI)-induced tumors are characterized by chromosomal instability (CIN); however, the mechanisms of this effect are unknown. We investigated the hypothesis that homologous recombination (HR) repair of DNA double strand breaks protect cells from Cr(VI)-induced CIN by focusing on the XRCC3 and RAD51C genes, which play an important role in cellular resistance to DNA double strand breaks. We used Chinese hamster cells defective in each HR gene (irs3 for RAD51C and irs1SF for XRCC3) and compared with their wildtype parental and cDNA-complemented controls. We found that the intracellular Cr ion levels varied among the cell lines after particulate chromate treatment. Importantly, accounting for differences in Cr ion levels, we discovered that XRCC3 and RAD51C cells treated with lead chromate had increased cytotoxicity and chromosomal aberrations, relative to wild-type and cDNA-complimented cells. We also observed the emergence of high levels of chromatid exchanges in the two mutant cell lines. For example, 1 ug/cm 2 lead chromate induced 20 and 32 exchanges in XRCC3-and RAD51C-deficient cells, respectively, whereas no exchanges were detected in the wildtype and cDNA-complemented cells. These observations suggest that HR protects cells from Cr(VI)-induced CIN, consistent with the ability of particulate Cr(VI) to induce double strand breaks.

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“…The tetrahedral anionic conformation of the +6 oxidation state of chromium facilitates active transport into cell systems through the phosphate and sulfate cellular transport systems (8). However, Cr(VI) is not the oxidation state that reacts with DNA, and cellular reduction of Cr(VI) to its stable +3 oxidation state forms a wide variety of intermediate high-valent (+4 and +5) oxidation states of chromium, as well as reductant-specific carbon-, oxygen-, and sulfurbased free radicals (9)(10)(11)(12). Both the high-valent chromium intermediates and free radicals have the potential to cause oxidative DNA damage promoted by Cr(VI).…”

Section: Introductionmentioning

confidence: 99%

Guanine-Specific Oxidation of Double-Stranded DNA by Cr(VI) and Ascorbic Acid Forms Spiroiminodihydantoin and 8-Oxo-2‘-deoxyguanosine

Slade

Hailer

Martin

et al. 2005

Chem. Res. Toxicol.

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7,8-dihydro-8-oxoguanine (8-oxoG) is thought to be a major lesion formed in DNA by oxidative attack at the nucleobase guanine. Recent studies have shown that 8-oxoG has a lower reduction potential than the parent guanine and is a hot spot for further oxidation. Spiroiminodihydantoin (Sp) has been identified as one of these further oxidation products. Chromium(VI) is a human carcinogen that, when reduced by a cellular reductant such as ascorbate, can oxidize DNA. In this study, duplex DNA was reacted with Cr(VI) and ascorbate to identify and quantify the base lesions formed. Guanine bases were observed to be preferentially oxidized with 5′ guanines within purine repeats showing enhanced oxidation. Trapping of the guanine lesions by the base excision repair enzymes hOGG1 and mNEIL2 showed nearly exclusive trapping by mNEIL2, suggesting that 8-oxoG was not the major lesion but rather a lesion recognized by mNEIL2 such as Sp. Formation of the Sp lesion in the Cr(VI)/Asc oxidation reaction with DNA was confirmed by LC-ESI-MS detection. HPLC-ECD was used to identify and quantify any 8-oxoG arising from Cr(VI)/Asc oxidation of DNA. Concentrations of Cr(VI) (3.1-50 μM) with a corresponding 1:10 ratio of Asc oxidized between 0.3% and 1.5% of all guanines within the duplex DNA strand to Sp. 8-oxoG was also identified but with the highest Cr (VI) concentration converting ~0.1% of all guanines to 8-oxoG. These results show that Sp was present in concentrations ~20 times greater than that of 8-oxoG in this system. The results indicate that 8-oxoG, while present, was not the major product of Cr(VI)/Asc oxidation of DNA and that Sp predominates under these conditions. These results further imply that Sp may be the lesion that accounts for the carcinogenicity of this metal in cellular systems.

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Effect of vitamin E on survival, glutathione reductase and formation of chromium (V) in Chinese hamster V-79 cells treated with sodium chromate (VI)

Cited by 79 publications

References 0 publications

Metal mutagenesis in transgenic Chinese hamster cell lines.

Metal mutagenesis in transgenic Chinese hamster cell lines.

Homologous recombination repair protects against particulate chromate-induced chromosome instability in Chinese hamster cells

Guanine-Specific Oxidation of Double-Stranded DNA by Cr(VI) and Ascorbic Acid Forms Spiroiminodihydantoin and 8-Oxo-2‘-deoxyguanosine

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