Induction of micronuclei in respiratory tract following radon inhalation

Brooks, Antone L.; Bao, Shijun; Harwood, Patrick W.; Wood, Barbara H.; Chrisler, William B.; Khan, Mohammed; Gies, Richard A.; Cross, F.T.

doi:10.1080/095530097142988

Cited by 19 publications

(1 citation statement)

References 17 publications

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“… 1997 ; Brooks et al. 1997 ). Aberration frequency per se in these tissues does not predict cancer: the same amount of chromosome damage results in a different frequency of cancer.…”

Section: Resultsmentioning

confidence: 99%

The role of dose rate in radiation cancer risk: evaluating the effect of dose rate at the molecular, cellular and tissue levels using key events in critical pathways following exposure to low LET radiation

Brooks

Hoel

Preston

2016

International Journal of Radiation Biology

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Purpose: This review evaluates the role of dose rate on cell and molecular responses. It focuses on the influence of dose rate on key events in critical pathways in the development of cancer. This approach is similar to that used by the U.S. EPA and others to evaluate risk from chemicals. It provides a mechanistic method to account for the influence of the dose rate from low-LET radiation, especially in the low-dose region on cancer risk assessment. Molecular, cellular, and tissues changes are observed in many key events and change as a function of dose rate. The magnitude and direction of change can be used to help establish an appropriate dose rate effectiveness factor (DREF). Conclusions: Extensive data on key events suggest that exposure to low dose-rates are less effective in producing changes than high dose rates. Most of these data at the molecular and cellular level support a large (2–30) DREF. In addition, some evidence suggests that doses delivered at a low dose rate decrease damage to levels below that observed in the controls. However, there are some data human and mechanistic data that support a dose-rate effectiveness factor of 1. In summary, a review of the available molecular, cellular and tissue data indicates that not only is dose rate an important variable in understanding radiation risk but it also supports the selection of a DREF greater than one as currently recommended by ICRP (2007) and BEIR VII (NRC/NAS 2006).

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“… 1997 ; Brooks et al. 1997 ). Aberration frequency per se in these tissues does not predict cancer: the same amount of chromosome damage results in a different frequency of cancer.…”

Section: Resultsmentioning

confidence: 99%

The role of dose rate in radiation cancer risk: evaluating the effect of dose rate at the molecular, cellular and tissue levels using key events in critical pathways following exposure to low LET radiation

Brooks

Hoel

Preston

2016

International Journal of Radiation Biology

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Micronucleus assay for mouse alveolar Type II and Clara cells

Lindberg

Falck

Catalán

et al. 2009

Environ and Mol Mutagen

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The objective of our study was to develop a micronucleus (MN) assay for detecting genotoxic damage after inhalation exposure in mouse alveolar Type II and Clara cells, potential target cells for lung carcinogens. Ten male C57BL/6J mice were exposed to ethylene oxide (630 mg/m(3)) for 4 hr via inhalation; 10 unexposed mice serving as controls. 72 hr after the exposure, Clara cells and alveolar Type II cells were isolated using two different methods. Method 1 included a 15-min trypsin lavage and a 2-hr incubation of cell suspension. Method 2 involved a 30-min trypsin lavage, Percoll gradient centrifugation, and a 48-hr incubation for cell attachment. Nitro blue tetrazolium (NBT) -staining was applied to distinguish Clara cells. The frequency of micronuclei (MNi) was scored in NBT-negative cells (defined as Type II cells in Method 2) and NBT-positive cells (Clara cells). To detect possible differences between the techniques, MNi in Clara cells were analyzed from samples prepared by both methods. With Method 2, a clear increase in the mean frequency of micronucleated cells was seen in the exposed mice as compared with the controls, for both alveolar Type II and Clara cells. However, no significant increase in MN frequency was seen in Clara cells analyzed from samples prepared by Method 1. Based on our findings, mouse alveolar Type II and Clara cells seem to be suitable for MN analysis in studies aimed at identifying genotoxic lung carcinogens. Both alveolar Type II and Clara cells can be isolated using Method 2.

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TP53 mutations in workers exposed to occupational carcinogens

Vähäkangas¹

2003

Hum. Mutat.

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For the p53 Special IssueIn some cases, evidence exists that exogenous carcinogenic exposures contribute to the mutation spectrum of the TP53 gene (p53) in human cancers. Although the clearest examples come from dietary and environmental sources, only a restricted number of papers have concentrated specifically on TP53 mutations in tumors from workers exposed to occupational carcinogens. In populations exposed to dietary aflatoxin B1 with liver cancer (AFB1) and ultraviolet (UV)-radiation with skin cancer, a single specific-looking TP53 mutation has been described in some of the tumors. Whether these fingerprints in the TP53 gene can be used to reveal an occupational etiology remains to be shown. In other cases, although differences in the TP53 mutation spectrum exist, they are more diffuse and difficult to interpret at this point. For instance, cigarette smoking seems to induce long-lasting molecular footprints in TP53. However, their use to rule out other occupational exposures as etiological factors in occupational cancers is still very questionable, especially due to the putative synergistic effects of cigarette smoke with other carcinogens. Although interesting implications of possible typical mutation spectra among cancers with other occupational etiologies exist, the data are scanty and await further development of TP53 mutation databases. Hum Mutat 21:240-251,

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Induction of micronuclei in respiratory tract following radon inhalation

Cited by 19 publications

References 17 publications

The role of dose rate in radiation cancer risk: evaluating the effect of dose rate at the molecular, cellular and tissue levels using key events in critical pathways following exposure to low LET radiation

The role of dose rate in radiation cancer risk: evaluating the effect of dose rate at the molecular, cellular and tissue levels using key events in critical pathways following exposure to low LET radiation

Micronucleus assay for mouse alveolar Type II and Clara cells

TP53 mutations in workers exposed to occupational carcinogens

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