Studies of mutagenesis and neoplastic transformation by bivalent metal ions and ionizing radiation

Little, John B.; Frenial, Jean-Michel; Coppey, Jacques

doi:10.1002/tcm.1770080505

Cited by 14 publications

(2 citation statements)

References 14 publications

(5 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This enhancement activity of nickel compounds may be due to their effect on DNA repair. On the other hand, no enhancement effect was detected in a CHO/ HGPRT gene mutation assay (26). Nevertheless, the mechanisms for the potential synergistic effects need to be elucidated.…”

Section: Introductionmentioning

confidence: 97%

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Heo²,

Chiewchanwit³

1994

Environ Health Perspect

View full text Add to dashboard Cite

Carcinogenic nickel compounds are usually found to be weak mutagens; therefore these compounds may not exert their carcinogenic activity through conventional genotoxic mechanisms. On the other hand, the activities of many nickel compounds have not been adequately investigated. We evaluated the genotoxic activities of nickel acetate using conventional chromosome aberration and sister chromatid exchange assays and found that there was no increase of chromosome aberrations or sister chromatid exchanges, although the highest dose (1000 pM) caused mitotic inhibition. In addition,. we investigated its effect on DNA repair using our challenge assay. In this assay, lymphocytes were exposed to 0.1 to 100 pM nickel acetate for 1 hr during the GO phase of the cell cycle. The cells were washed free of the chemical and, 1.5 hr later, were irradiated with two doses of y-rays (75 cGy per dose separated by 60 min). A significant dose-dependent increase of chromosome translocations was observed (p<0.05). The increase is more than expected based on additive effects from exposure to nickel or trays individually. In contrast to the increase of chromosome translocations, there was no increase in chromosome deletions, although there was a nickel dose-dependent reduction of mitotic indices. Our data suggest that pretreatment with nickel interferes with the repair of radiation-induced DNA damage and potentially cause mistakes in DNA repair. Furthermore, we suggest that nickel-induced abnormal DNA repair may be a mechanism for its carcinogenic properties. The DNA repair problems that we observed after exposure to low doses of nickel may be viewed as a type of adaptive response. Contrary to some investigators who showed that adaptive responses may be beneficial, our data indicated that some responses may cause more problems than expected.-Environ Health Perspect 102(Suppl 9): 73-77 (1994)

show abstract

Section: Introductionmentioning

confidence: 97%

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Heo²,

Chiewchanwit³

1994

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…The HPRT mutation assay is a method commonly used to study the genetic changes and genomic instability [ 19 , 20 ]. After irradiation, the culture medium was removed, and the cells were washed twice with PBS.…”

Section: Methodsmentioning

confidence: 99%

X-ray-induced bystander responses reduce spontaneous mutations in V79 cells

Maeda¹,

Kobayashi²,

Matsumoto³

et al. 2013

Journal of Radiation Research

View full text Add to dashboard Cite

The potential for carcinogenic risks is increased by radiation-induced bystander responses; these responses are the biological effects in unirradiated cells that receive signals from the neighboring irradiated cells. Bystander responses have attracted attention in modern radiobiology because they are characterized by non-linear responses to low-dose radiation. We used a synchrotron X-ray microbeam irradiation system developed at the Photon Factory, High Energy Accelerator Research Organization, KEK, and showed that nitric oxide (NO)-mediated bystander cell death increased biphasically in a dose-dependent manner. Here, we irradiated five cell nuclei using 10 × 10 µm2 5.35 keV X-ray beams and then measured the mutation frequency at the hypoxanthine-guanosine phosphoribosyl transferase (HPRT) locus in bystander cells. The mutation frequency with the null radiation dose was 2.6 × 10–5 (background level), and the frequency decreased to 5.3 × 10–6 with a dose of approximately 1 Gy (absorbed dose in the nucleus of irradiated cells). At high doses, the mutation frequency returned to the background level. A similar biphasic dose-response effect was observed for bystander cell death. Furthermore, we found that incubation with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), a specific scavenger of NO, suppressed not only the biphasic increase in bystander cell death but also the biphasic reduction in mutation frequency of bystander cells. These results indicate that the increase in bystander cell death involves mechanisms that suppress mutagenesis. This study has thus shown that radiation-induced bystander responses could affect processes that protect the cell against naturally occurring alterations such as mutations.

show abstract

Manganese and its inorganic compounds [MAK Value Documentation, 1999]

2012

The MAK‐Collection for Occupational Health and Safety

View full text Add to dashboard Cite

Published in the series Occupational Toxicants , Vol. 12 (1999) The article contains sections titled: Occurrence, Production and Use Exposure Assay procedures Manganese concentrations at the workplace Toxic Effects and Mode of Action Mechanism of Action Toxicokinetics Uptake Distribution, accumulation Excretion Biomonitoring Effects in Man Single exposures Multiple exposures Effects on skin and mucous membranes Allergenic effects Reproductive and Developmental Toxicity Carcinogenicity Effects on Animals Acute toxicity Subacute, subchronic and chronic toxicity Reproductive and Developmental Toxicity Genotoxicity Carcinogenicity Other effects Manifesto (MAK value, classification)

show abstract

Studies of mutagenesis and neoplastic transformation by bivalent metal ions and ionizing radiation

Cited by 14 publications

References 14 publications

Toxicological interactions between nickel and radiation on chromosome damage and repair.

Toxicological interactions between nickel and radiation on chromosome damage and repair.

X-ray-induced bystander responses reduce spontaneous mutations in V79 cells

Manganese and its inorganic compounds [MAK Value Documentation, 1999]

Contact Info

Product

Resources

About