Induction of congenital malformations in the offspring of male mice treated with X-rays at pre-meiotic and post-meiotic stages

Kirk, Maggie; Mf, Lyon

doi:10.1016/0027-5107(84)90034-4

Cited by 127 publications

(25 citation statements)

References 15 publications

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“…The DL method has been instrumental in identifying numerous mutagenic agents since its inception (Luning & Searle, 1971;Searle & Beechey, 1981;Kirk & Lyon, 1984). Yet, since the DL assay is primarily employed to discover mutagens that cause chromosomal aberrations using embryonic death functions as the end-point, the assay fails to provide a definitive outcome, considering that additional genetic events and environmental factors may also heavily influence the occurrence of in utero loss of embryos.…”

Section: Dominant Lethal Testmentioning

confidence: 99%

The effects of extremely low frequency magnetic fields on mutation induction in mice

Wilson

Haines

Sienkiewicz

et al. 2015

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Section: Dominant Lethal Testmentioning

confidence: 99%

The effects of extremely low frequency magnetic fields on mutation induction in mice

Wilson

Haines

Sienkiewicz

et al. 2015

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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“…Similarities between man and rodents in the process of spermatogenesis indicate that studies in animals can help us understand the mechanisms of male-mediated teratogenesis in man. In animal studies, paternal exposure to numerous agents including environmental chemicals has been shown to cause congenital malformations (Nomura, 1975(Nomura, , 1982Kirk and Lyon, 1984;Nagao, 1987Nagao, , 1988Nagao, , 1999Nagao and Fujikawa, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Over the twenty years since the pioneering work of Nomura (1975), it has become clear that preconceptual exposure of paternal animals to chemical or physical agents can cause congenital malformations in the offspring. Recently, a number of animal studies as well as human epidemiological studies have demonstrated that exposure of males to various agents can result in developmental defects or phenotypic anomalies (Jenkinson et al, 1987;Jenkinson and Anderson, 1990; Kirk and Lyon, 1984;Nagao, 1987Nagao, , 1988Nagao, , 1994Nagao and Fujikawa, 1990;Trasler et al, 1985Trasler et al, , 1986.…”

Section: T Nagaomentioning

confidence: 99%

Male‐Mediated Developmental Toxicity: Enhanced Susceptibility to Induced Teratogenesis in the Offspring of Male Mice Treated with Ethylnitrosourea

Nagao

1999

Congenital Anomalies

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Male ICR strain mice were injected intraperitoneally with ENU at 50 mg/kg daily for 5 days and mated to untreated virgin females of the same strain on days 64-80 after the last dose. Copulations during this period involved spermatogonial stem cells at the time of the last treatment. Subsequently, copulated females were injected intraperitoneally with ENU at 25-100 mg/kg on day 8 of gestation, at 50-200 mg/kg on day 12 of gestation or injected subcutaneously with triamcinolone acetonide at 1.25-10 m g k g on day 12 of gestation. The uterine contents were examined on day 18 of gestation. Fetuses of dams treated on day 8 of gestation were inspected for external and skeletal abnormalities, and those of dams treated on day 12 were inspected for external abnormalities including cleft palate. Frequencies of microphthalmia and cleft palate in the group in which females mated with ENU-treated males were treated with ENU at 50 mg/kg on day 8 of gestation or with ENU at 50 mg/kg on day 12 of gestation, respectively, were significantly higher than those in the group in which females mated with phosphate buffer-treated males were treated with ENU at 50 mgkg on day 8 or at 50 mg/kg on day 12. No significant increases in the frequency of cleft palate were observed in the groups in which females mated with ENUtreated males were treated with triamcinolone acetonide on day I : ! of gestation as compared with groups in which females mated with phosphate buffer-treated males were treated with triamcinolone acetonide on day 12 of gestation. These results suggested the increased susceptibility to induced teratogenesis (congenital malformations induced by exposure of embryo/fetus during gestation) in the offspring derived from paternal germ cells treated with the potent mutagen ENU, but not the non-mutagen triamcinolone acetonide.

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“…From animal experiments it was anticipated that paternal exposure to radiation and chemicals would induce F, congenital malformations in the offspring of ICR mice [l-31 and of (C3H/HeH x 101/H) F, mice [4,5]. We confirmed these findings in our own studies in which various kinds of chemicals were comparatively assayed for their genotoxic potentials in the spermatogonial stem cells of ICR mice [6-91 and C57BL/6 mice [ 101 using F, congenital malformations as endpoints.…”

Section: Introductionmentioning

confidence: 99%

Male-mediated teratogenesis: Spectrum of congenital malformations in the offspring of A/J male mice treated with ethylnitrosourea

Nagao

Fujikawa

1996

Teratog. Carcinog. Mutagen.

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Induction of congenital malformations in the offspring of male mice treated with X-rays at pre-meiotic and post-meiotic stages

Cited by 127 publications

References 15 publications

The effects of extremely low frequency magnetic fields on mutation induction in mice

The effects of extremely low frequency magnetic fields on mutation induction in mice

Male‐Mediated Developmental Toxicity: Enhanced Susceptibility to Induced Teratogenesis in the Offspring of Male Mice Treated with Ethylnitrosourea

Male-mediated teratogenesis: Spectrum of congenital malformations in the offspring of A/J male mice treated with ethylnitrosourea

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