Arsenic[III] and heavy metal ions induce intrachromosomal homologous recombination in thehprt gene of V79 Chinese hamster cells

Helleday, Thomas; Nilsson, Robert; Jenssen, Dag

doi:10.1002/(sici)1098-2280(2000)35:2<114::aid-em6>3.0.co;2-q

Cited by 57 publications

(32 citation statements)

References 33 publications

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“…In addition, the majority of the CD59 Ϫ mutants induced were caused by multilocus deletions of several million base pairs. Our data are consistent with the recent report that arsenic induces intrachromosomal recombination in the HPRT gene of Chinese hamster ovary cells (23). Biologically, the trivalent sodium arsenite is significantly more active than the pentavalent sodium arsenate, including the ability to induce gene amplification in mammalian cells (17,24).…”

supporting

confidence: 93%

Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity

Liu

Athar

Lippai

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

430

192

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Although arsenic is a well-established human carcinogen, the mechanisms by which it induces cancer remain poorly understood. We previously showed arsenite to be a potent mutagen in humanhamster hybrid (AL) cells, and that it induces predominantly multilocus deletions. We show here by confocal scanning microscopy with the fluorescent probe 5,6-chloromethyl-2,7-dichlorodihydrofluorescein diacetate that arsenite induces, within 5 min after treatment, a dose-dependent increase of up to 3-fold in intracellular oxyradical production. Concurrent treatment of cells with arsenite and the radical scavenger DMSO reduced the fluorescent intensity to control levels. ESR spectroscopy with 4-hydroxy-2,2,6,6-tetramethyl-1-hydroxypiperidine (TEMPOL-H) as a probe in conjunction with superoxide dismutase and catalase to quench superoxide anions and hydrogen peroxide, respectively, indicates that arsenite increases the levels of superoxide-driven hydroxyl radicals in these cells. Furthermore, reducing the intracellular levels of nonprotein sulfhydryls (mainly glutathione) in A L cells with buthionine S-R-sulfoximine increases the mutagenic potential of arsenite by more than 5-fold. The data are consistent with our previous results with the radical scavenger DMSO, which reduced the mutagenicity of arsenic in these cells, and provide convincing evidence that reactive oxygen species, particularly hydroxyl radicals, play an important causal role in the genotoxicity of arsenical compounds in mammalian cells.

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supporting

confidence: 93%

Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity

Liu

Athar

Lippai

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

430

192

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“…A large number of researches show that human peripheral blood lymphocytes hypoxantine-guanine phpsphoribosyl transferase (HPRT) gene, which is a chemical and ionizing radiation sensitive mutagen loci (Nicklas et al, 1991;Zimmer et al, 1997;Hamdan et al, 1999;Helleday et al, 2000), was closely related to the p53 and bcl-2 gene (Liu et al, 1997;Phillips, Gebow et al, 1997), which had been demonstrated strongly association with cancer development (Murray et al, 2012;Zeestraten et al, 2013),especially with breast cancer and esophageal cancer (Bellini et al, 2012;Walerych et al, 2012). Therefore, it is worthy to emphasize that the occupational X-ray radiation exposure might interact with phosphoribosyl gene mutation contribute to cancer susceptibility.…”

Section: Discussionmentioning

confidence: 99%

Nested Case-control Study of Occupational Radiation Exposure and Breast and Esophagus Cancer Risk among Medical Diagnostic X Ray Workers in Jiangsu of China

Wang

Fang²,

Tang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Medical diagnostic X-ray workers are one occupational group that expose to the long-term low-dose external radiation over their working lifetime, and they may under risk of different cancers. This study aims to determine the relationship between the occupational X-ray radiation exposure and cancer risk among these workers in Jiangsu, China. We conducted Nested case-control study to investigate the occupational X-ray radiation exposure and cancer risk. Data were collected through self-administered questionnaire, which includes but not limits to demographic data, personal behaviors and family history of cancer. Retrospective dose reconstruction was conducted to estimate the cumulative doses of the x-ray workers. Inferential statistics, t-test and 2 tests were used to compare the differences between each group. We used the logistic regression model to calculate the odds ratio (OR) and 95% confidence interval (CI) of cancer by adjusting the age, gender. All 34 breast cancer cases and 45 esophageal cancer cases that detected in a cohort conducted among health workers between 1950~2011 were included in this presented study, and 158 cancer-free controls were selected by frequency-matched (1:2). Our study found that the occupational radiation exposure was associated with a significantly increased cancer risk compared with the control, especially in breast cancer and esophageal cancer (adjusted OR=2.90, 95% CI: 1.19-7.04 for breast cancer; OR=4.19, 95% CI: 1.87-9.38 for esophageal cancer, and OR=3.43, 95% CI: 1.92-6.12 for total cancer, respectively). The occupational X-ray radiation exposure was associated with increasing cancer risk, which indicates that proper intervention and prevention strategies may be needed in order to bring down the occupational cancer risk.

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“…Cr(VI)-induced DNA single strand breaks appear when DNA is isolated under alkaline conditions (26). Despite the wide range of DNA damage induced by Cr(VI), no evidence has linked Cr(VI) to direct DSB formation; however, Cr(VI) is a potent inducer of recombination (27). We have shown that Cr(VI) exposure results in activation of p53 (28) and that Cr(VI)-induced apoptosis is p53-dependent (29).…”

mentioning

confidence: 99%

Chromium (VI) Activates Ataxia Telangiectasia Mutated (ATM) Protein

Ceryak

Patierno

2003

Journal of Biological Chemistry

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The ataxia telangiectasia mutated (ATM) protein plays a central role in early stages of DNA double strand break (DSB) detection and controls cellular responses to this damage. Although hypersensitive to ionizing radiation-induced clonogenic lethality, ataxia telangiectasia cells are paradoxically deficient in their ability to undergo ionizing radiation-induced apoptosis. This contradiction illustrates the complexity of the central role of ATM in DNA damage response and the need for further understanding. Certain hexavalent chromium (Cr(VI)) compounds are implicated as occupational respiratory carcinogens at doses that are both genotoxic and cytotoxic. Cr(VI) induces a broad spectrum of DNA damage, but Cr(VI)-induced DSBs have not been reported. Here, we examined the role of ATM in the cellular response to Cr(VI) and found that Cr(VI) activates ATM. We also show that physiological targets of ATM, p53 Ser-15 and Chk2 Thr-68, were phosphorylated by Cr(VI) exposure in an ATM-dependent fashion. We found that ATM؊/؊ cells were markedly resistant to Cr(VI)-induced apoptosis but considerably more sensitive to Cr(VI)-induced clonogenic lethality than wild type cells, indicating that resistance to Cr(VI)-induced apoptosis did not confer a selective survival advantage. However, analysis of long term growth arrest revealed a striking difference: ATM؊/؊ cells were markedly less able to recover from Cr(VI)-induced growth arrest. This indicates that terminal growth arrest is the fate of these apoptosis-resistant cells. In summary, ATM is involved in cellular response to a complex genotoxin that may not directly induce DSBs. Our data suggest that ATM is a major signal initiator for genotoxin-induced apoptosis but, paradoxically, also contributes to maintenance of cell survival by facilitating recovery/escape from terminal growth arrest. The results also strongly suggest that terminal growth arrest is not merely an extended or even irreversible form of checkpoint arrest, but instead an independent and unique cell fate pathway.

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Arsenic[III] and heavy metal ions induce intrachromosomal homologous recombination in thehprt gene of V79 Chinese hamster cells

Cited by 57 publications

References 33 publications

Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity

Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity

Nested Case-control Study of Occupational Radiation Exposure and Breast and Esophagus Cancer Risk among Medical Diagnostic X Ray Workers in Jiangsu of China

Chromium (VI) Activates Ataxia Telangiectasia Mutated (ATM) Protein

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