Use of the frequencies of micronuclei as quantitative indicators of X-ray-induced chromosomal aberrations in human peripheral blood lymphocytes: Comparison of two methods

Ramalho, A.T.; Šunjevarić, Ivana; Natarajan, A.T.

doi:10.1016/0165-7992(88)90078-4

Cited by 119 publications

(29 citation statements)

References 7 publications

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“…If one restricts scoring to micronuclei in binucleated cells, it is possible to accurately estimate the frequencies. The dose-response curve for induction of micronuclei in human lymphocytes induced by X-rays is curvilinear, indicating that part of the micronuclei arise from the acentrics associated with two-hit events, i.e., dicentrics (19). A parallel analysis of chromosome aberrations and micronuclei in irradiated lymphocytes indicated that about 70-90% of fragments form micronuclei at low radiation doses (up to 2 Gy), whereas at higher doses about 40% of fragments formed micronuclei (19).…”

Section: Chromosomal Alterationsmentioning

confidence: 90%

“…The dose-response curve for induction of micronuclei in human lymphocytes induced by X-rays is curvilinear, indicating that part of the micronuclei arise from the acentrics associated with two-hit events, i.e., dicentrics (19). A parallel analysis of chromosome aberrations and micronuclei in irradiated lymphocytes indicated that about 70-90% of fragments form micronuclei at low radiation doses (up to 2 Gy), whereas at higher doses about 40% of fragments formed micronuclei (19). This low efficiency of the micronucleus technique at higher radiation doses appears to be due to the facts that a) some of the fragments are included into the main nuclei and b) cells carrying no or a lower number of fragments divide earlier than highly affected cells.…”

Section: Chromosomal Alterationsmentioning

confidence: 99%

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Mechanisms for induction of mutations and chromosome alterations.

Natarajan

1993

Environ Health Perspect

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Genotoxic agents induce chromosomal alterations, such as aberrations, micronuclei, and sister chromatid exchanges as well as mutations both in vivo and in vitro. Ionizing radiation and typical radiomimmetic agents such as bleomycin are very efficient inducers of chromosomal aberrations. The type of aberrations induced by these agents are cell-cycle dependent, i.e., chromosome type in pre-replication stages and chromatid type in post-replication stages of the cell cycle. Under optimal DNA repair conditions, DNA double-strand breaks (DSBs) appear to be the most important lesion responsible for the production of aberrations. In human lymphocytes, fast-repairing DSBs lead to exchange-type aberrations. The fact that the dose-response curves for induction of exchange aberrations induced by ionizing radiation are similar in vitro and in vivo allows one to use the yield of induced aberrations to estimate absorbed radiation dose in the case of accidents. In this respect, frequencies of translocations detected by the chromosome painting technique appear to be more sensitive. Mutations do not express immediately after exposure and require an expression time before they can be detected. In humans, it is estimated that for the mutations induced in bone marrow, it takes about 2 months for them to express and to be detected in peripheral blood lymphocytes. Hence, frequency of mutations is of limited value for estimating radiation doses immediately after an accident. This holds true for chemical exposure as well. Most of the lesions induced by chemical mutagens (such as alkylating agents) are converted into aberrations only during the S phase of the cell cycle, and therefore an intervening DNA synthesis following exposure is necessary for the visualization of aberrations. These agents induce mainly the chromatid-type aberrations and are also very efficient in inducing sister chromatid exchanges. Chemical mutagens are more efficient in inducing gene mutations than ionizing radiations. In monitoring human populations, mutations in the hprt locus in peripheral lymphocytes and hemoglobin mutations as well as glycophorin mutations in erythrocytes can be studied. The hprt mutations and glycophorin mutations can arise from single base-pair changes to large deletions, whereas hemoglobin mutations arise from changes in a single codon.

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Section: Chromosomal Alterationsmentioning

confidence: 90%

Section: Chromosomal Alterationsmentioning

confidence: 99%

Mechanisms for induction of mutations and chromosome alterations.

Natarajan

1993

Environ Health Perspect

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“…A negative correlation was observed between MN induction and cell proliferation; the higher the MN frequency detected in exposed individuals, the lower the values of nuclear division progression expressed as RI. In living creatures, which are exposed to a mutagen factor, the probability of formation of mitotic and meiotic defects is increased and the rate of MN could increase due to this increase (Ramalho et al 1988). This may mean that cells with greater chromosomal damage may die before cell division or may be less capable to enter this phase (Santos-Mello et al, 1974).…”

Section: Plant Extracts As Cytotoxic Agentsmentioning

confidence: 99%

Potential Genotoxic and Cytotoxic Effects of Plant Extracts

Çelik¹

2012

A Compendium of Essays on Alternative Therapy

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“…The intercellular distribution of MN has been reported to be Poisson (Ramalho et al 1988;Littlefield et al 1989) or hyperPoisson (Prosser et al 1988), or over-dispersed (Hoffmann et al 1993;Vral et al 1994), depending on the radiation dose. While the frequencies of MN and acentric fragments increasingly diverge at doses of sparsely ionizing radiation above 1 Gy, it appears that at low doses of this type of radiation virtually all acentric fragments can be recovered as MN (Ramalho et al 1988;Littlefield et al 1989;Vral et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Evidence for Radiation Hormesis after In Vitro Exposure of Human Lymphocytes to Low Doses of Ionizing Radiation

Rithidech

Scott

2008

Dose-Response

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h Previous research has demonstrated that adding a very small gamma-ray dose to a small alpha radiation dose can completely suppress lung cancer induction by alpha radiation (a gamma-ray hormetic effect). Here we investigated the possibility of gamma-ray hormesis during low-dose neutron irradiation, since a small contribution to the total radiation dose from neutrons involves gamma rays. Using binucleated cells with micronuclei (micronucleated cells) among in vitro monoenergetic-neutron-irradiated human lymphocytes as a measure of residual damage, we investigated the influence of the small gammaray contribution to the dose on suppressing residual damage. We used residual damage data from previous experiments that involved neutrons with five different energies (0.22-, 0.44-, 1.5-, 5.9-, and 13.7-million electron volts [MeV]). Corresponding gamma-ray contributions to the dose were approximately 1%, 1%, 2%, 6%, and 6%, respectively. Total absorbed radiation doses were 0, 10, 50, and 100 mGy for each neutron source. We demonstrate for the first time a protective effect (reduced residual damage) of the small gamma-ray contribution to the neutron dose. Using similar data for exposure to gamma rays only, we also demonstrate a protective effect of 10 mGy (but not 50 or 100 mGy) related to reducing the frequency of micronucleated cells to below the spontaneous level.

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Use of the frequencies of micronuclei as quantitative indicators of X-ray-induced chromosomal aberrations in human peripheral blood lymphocytes: Comparison of two methods

Cited by 119 publications

References 7 publications

Mechanisms for induction of mutations and chromosome alterations.

Mechanisms for induction of mutations and chromosome alterations.

Potential Genotoxic and Cytotoxic Effects of Plant Extracts

Evidence for Radiation Hormesis after In Vitro Exposure of Human Lymphocytes to Low Doses of Ionizing Radiation

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