Nickel subsulfide is similar to potassium dichromate in protecting normal human fibroblasts from the mutagenic effects of benzo[a]pyrene diolepoxide

Hamdan, Samir M.; Morse, Brent; Reinhold, David S.

doi:10.1002/(sici)1098-2280(1999)33:3<211::aid-em5>3.0.co;2-7

Cited by 12 publications

(7 citation statements)

References 34 publications

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“…No colonies were observed at 50 μM iAs III . The colony-forming assay is known to be a very sensitive method of toxicity evaluation, but it may underestimate early cell survival (Hamdan et al 1999). …”

Section: Resultsmentioning

confidence: 99%

Elevation of Cellular BPDE Uptake by Human Cells: A Possible Factor Contributing to Co-Carcinogenicity by Arsenite

Shen¹,

Lee

Sun

et al. 2006

Environ Health Perspect

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BackgroundArsenite (iAsIII) can promote mutagenicity and carcinogenicity of other carcinogens. Considerable attention has focused on interference with DNA repair by inorganic arsenic, especially the nucleotide excision repair (NER) pathway, whereas less is known about the effect of arsenic on the induction of DNA damage by other agents.ObjectivesWe examined how arsenic modulates DNA damage by other chemicals.MethodsWe used an NER-deficient cell line to dissect DNA damage induction from DNA repair and to examine the effects of iAsIII on the formation of benzo[a]pyrene diol epoxide (BPDE)–DNA adducts.ResultsWe found that pretreatment with iAsIII at subtoxic concentrations (10 μM) led to enhanced formation of BPDE–DNA adducts. Reduced glutathione levels, glutathione S-transferase activity and chromatin accessibility were also measured after iAsIII treatment, but none of these factors appeared to account for the enhanced formation of DNA adducts. However, we found that pretreatment with iAsIII increased the cellular uptake of BPDE in a dose-dependent manner.ConclusionsOur results suggest that iAsIII enhanced the formation of BPDE–DNA adducts by increasing the cellular uptake of BPDE. Therefore, the ability of arsenic to increase the bioavailability of other carcinogens may contribute to arsenic co-carcinogenicity.

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Section: Resultsmentioning

confidence: 99%

Elevation of Cellular BPDE Uptake by Human Cells: A Possible Factor Contributing to Co-Carcinogenicity by Arsenite

Shen¹,

Lee

Sun

et al. 2006

Environ Health Perspect

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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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“…With regard to nickel, its carcinogenesis and mutagenicity have been previously reported (Hong et al . 1997; Hamdan et al . 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Although the reason for this is not clear, this metal ion strongly influences the cell viability of ES-D3 cells. With regard to nickel, its carcinogenesis and mutagenicity have been previously reported (Hong et al 1997;Hamdan et al 1999). The damage to the cells is caused at the genetic level by oxidation.…”

Section: Discussionmentioning

confidence: 99%

In vitro embryotoxicity testing of metals for dental use by differentiation of embryonic stem cell test

Imai

Nakamura

2006

Congenital Anomalies

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We examined embryotoxicity using the embryonic stem cell test (EST) protocol. Tests were conducted using standard reagents for the atomic absorption measurement of 11 metal ions, silver, cobalt, chromium, copper, mercury, nickel, palladium, antimony, tin, vanadium, and zinc from among metals comprising dental alloys. In addition, for four metals like silver, cobalt, chromium, and nickel, the tests were also conducted using a test solution extracted from powder in the cell culture medium. The embryotoxic potential was obtained from a biostatistics-based prediction model, which was calculated from three endpoints, the ID50, IC50ES and IC(50)3T3. Data with the standard reagents showed that chromium and mercury ions corresponded to class 3, that is, having a strong embryotoxicity, while antimony, tin, and vanadium ions exhibited a weak embryotoxicity. The other metal ions demonstrated no embryotoxicity. On the other hand, when extracts of metal powder in cell culture solutions were used, silver exhibited a weak embryotoxicity while all other metals exhibited no embryotoxicity. In the future, it will be important to clarify the embryotoxicity of the many dental materials that are in use today. In addition, it is necessary to develop substances to ensure they have no toxicity before use in dental applications.

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Nickel subsulfide is similar to potassium dichromate in protecting normal human fibroblasts from the mutagenic effects of benzo[a]pyrene diolepoxide

Cited by 12 publications

References 34 publications

Elevation of Cellular BPDE Uptake by Human Cells: A Possible Factor Contributing to Co-Carcinogenicity by Arsenite

Elevation of Cellular BPDE Uptake by Human Cells: A Possible Factor Contributing to Co-Carcinogenicity by Arsenite

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

In vitro embryotoxicity testing of metals for dental use by differentiation of embryonic stem cell test

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