Frequency and Type of Malformations in the Offspring of C57BL/6 Male Mice Treated with Ethylnitrosourea

Nagao, Tetsuji; Fujikawa, Kazuo

doi:10.1111/j.1741-4520.1996.tb00318.x

Cited by 3 publications

(1 citation statement)

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“…Direct study of chemically-induced transmitted genetic eŠects in humans is virtually impossible, so the genetic risk must be estimated from animal experiments. Congenital malformations can be induced in the oŠspring of laboratory animals exposed to environmental mutagens before copulation (1)(2)(3)(4)(5)(6). The spectra of congenital malformations in the oŠspring classiˆed as male-mediated malformations after exposure of paternal mice to mutagens showed no evidence of mutagen-speciˆcity or a germ-cell stage-dependent variation.…”

Section: Introductionmentioning

confidence: 99%

Transgenerational Teratogenesis by Prenatal Exposure to Endocrine Disrupting Chemicals

Nagao

Takada

Onoda

2011

Genes and Environment

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Section: Introductionmentioning

confidence: 99%

Transgenerational Teratogenesis by Prenatal Exposure to Endocrine Disrupting Chemicals

Nagao

Takada

Onoda

2011

Genes and Environment

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Modified Susceptibility to Teratogenesis in the Offspring of Male Mice Exposed to Mutagens

Nagao

Fujikawa

1998

Congenital Anomalies

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Preconceptual exposure of male mice to a mutagen can increase the incidence of malformations in the offspring. In mutagenized spermatogonial stem cells, genetic changes responsible for F1 malformations were produced in a manner similar to that involved in the production of specific locus mutations. Irrespective of the kind of mutagens applied, the germ cell stage treated and the strain of mice used, resulting F1 malformations showed type distributions that were indistinguishable from the spectrum of those occurring spontaneously. When a teratogen was applied at the organogenic stage, embryos whose sires were preconceptually exposed to a mutagen showed higher susceptibility to induced malformations than those derived from untreated males. Experimental results pertaining to these contentions are summarized and the possible implications are discussed.

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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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Frequency and Type of Malformations in the Offspring of C57BL/6 Male Mice Treated with Ethylnitrosourea

Cited by 3 publications

References 10 publications

Transgenerational Teratogenesis by Prenatal Exposure to Endocrine Disrupting Chemicals

Transgenerational Teratogenesis by Prenatal Exposure to Endocrine Disrupting Chemicals

Modified Susceptibility to Teratogenesis in the Offspring of Male Mice Exposed to Mutagens

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

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