Mechanisms of chromosomal aberration production II. Aberrations induced by 5-bromodeoxyuridine and visible light

Bender, Michael A.; Bedford, Joel S.; Mitchell, James B.

doi:10.1016/0027-5107(73)90061-4

Cited by 55 publications

(4 citation statements)

References 20 publications

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“…It is generally assumed that gaps are sites of despiralisation in the metaphase chromosome, which render the DNA invisible under light microscopy. It has been proposed that an achromatic lesion may actually be a single-strand break in the DNA double helix because of incomplete excision repair and thus may represent a point of possible instability [ 28 ]. Therefore, gaps are always noted but reported separately from true chromosomal aberrations.…”

Section: Methodsmentioning

confidence: 99%

Utility of Dexrazoxane for the Attenuation of Epirubicin-Induced Genetic Alterations in Mouse Germ Cells

et al. 2016

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Dexrazoxane has been approved to treat anthracycline-induced cardiomyopathy and extravasation. However, the effect of dexrazoxane on epirubicin-induced genetic alterations in germ cells has not yet been reported. Thus, the aim of this study was to determine whether dexrazoxane modulates epirubicin-induced genetic damage in the germ cells of male mice. Our results show that dexrazoxane was not genotoxic at the tested doses. Furthermore, it protected mouse germ cells against epirubicin-induced genetic alterations as detected by the reduction in disomic and diploid sperm, spermatogonial chromosomal aberrations, and abnormal sperm heads. The attenuating effect of dexrazoxane was greater at higher dose, indicating a dose-dependent effect. Moreover, sperm motility and count were ameliorated by dexrazoxane pretreatment. Epirubicin induced marked biochemical changes characteristic of oxidative DNA damage including elevated 8-hydroxy-2ʹ-deoxyguanosine levels and reduction in reduced glutathione. Pretreatment of mice with dexrazoxane before epirubicin challenge restored these altered endpoints. We conclude that dexrazoxane may efficiently mitigate the epirubicin insult in male germ cells, and prevent the enhanced risk of abnormal reproductive outcomes and associated health risks. Thus, pretreating patients with dexrazoxane prior to epirubicin may efficiently preserve not only sperm quality but also prevent the transmission of genetic damage to future generations.

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Section: Methodsmentioning

confidence: 99%

Utility of Dexrazoxane for the Attenuation of Epirubicin-Induced Genetic Alterations in Mouse Germ Cells

et al. 2016

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“…This evidence was also provided by Brewen et al (1975) who showed that the broken chromosomes due to the mutagenic action of chemical mutagen were eventually lost at anaphase, resulting in the death of the developing embryo. Bender et al (1973Bender et al ( , 1974 proposed a model by which chromosomal aberrations could be induced by a mutagen in the germ cells. Their studies strongly supported the view that the dominant lethality was the outcome of the loss of chromosomal material by way of deletions in the chromosomes of gametes.…”

Section: Resultsmentioning

confidence: 99%

Evaluation of mutagenic potential of acetamiprid by dominant lethal test on Culex quinquefasciatus

Bansal

Chaudhry

2011

JANS

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Acetamiprid, a member of the neonicotinoid insecticide family, is a new class of insecticide which has recently entered the market place. It is very selective and provides outstanding control of sucking pests such as aphids and whiteflies of major crops. In the present investigation, dominant lethal test (DLT) is adopted for the evaluation of the genotoxic effects of acetamiprid using Culex quinquefasciatus as an experimental model. In this experiment, the males hatched from larvae treated with LD 40 were cross mated with normal females and the results were based on the number of hatched and unhatched eggs laid by these females. The statistical analysis of the results for LD 40 treated groups gave the values of 37.526±3.886 as against 5.23±0.77 from the nontreated groups which indicated significant dominant lethality of p<0.01. These results indicated that exposure of pesticides even at small dose level proved deleterious to the genome of mosquito and its subsequent generation.

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“…When psoralin treated cells are exposed t6 visible light, DNA lesions, believed to be mainly interstrand crosslinks, are produced, and chromosomal aberrations result. Since the crosslinking is light-dependant, the lesion can be induced at known stages in the cell cycle in synchronized cultures, and an analysis analogous to those we performed earlier for 5-bromodeoxyuridine-plus-light-induced polynucleotide strand breaks (Bender, Bedford and Mitchell, 1973) and for ultraviolet-induced pyrimidine cyclobutane dimers (Bender, Griggs and Walker, 1973) is feasible.…”

Section: Chemical Clastogenesis Preliminary Experiments•and Observatmentioning

confidence: 98%

Mechanisms of aberration production in eukaryote chromosomes. Final report, July 1, 1973--June 30, 1975

Bender¹

1975

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Mechanisms of chromosomal aberration production II. Aberrations induced by 5-bromodeoxyuridine and visible light

Cited by 55 publications

References 20 publications

Utility of Dexrazoxane for the Attenuation of Epirubicin-Induced Genetic Alterations in Mouse Germ Cells

Utility of Dexrazoxane for the Attenuation of Epirubicin-Induced Genetic Alterations in Mouse Germ Cells

Evaluation of mutagenic potential of acetamiprid by dominant lethal test on Culex quinquefasciatus

Mechanisms of aberration production in eukaryote chromosomes. Final report, July 1, 1973--June 30, 1975

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