Dose response study for 1,3-butadiene-induced dominant lethal mutations and heritable translocations in germs cells of male mice

Adler, I.‐D.; Filser, Johannes G.; Gonda, H.; Schriever‐Schwemmer, G.

doi:10.1016/s0027-5107(97)00198-x

Cited by 18 publications

(4 citation statements)

References 17 publications

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“…Gray boxes represent period of sterility induced after exposure. Original data was presented in the following works (listed by mutagen): acrylamide (Shelby et al, 1986, 1987; Adler et al, 1994a), busulfan (Ehling and Neuhauser‐Klaus, 1991), benzo[a]pyrene (Generoso et al, 1982), 1,3‐butadiene (Adler et al, 1998), chlormbucil (Generoso et al, 1995), chlormethine (Fox and Scott, 1980; Ehling and Neuhauser‐Klaus, 1989), cyclophosphamide (Sotomayor and Cumming, 1975; Ehling and Neuhäuser‐Klaus, 1988), dacarbazine (Adler et al, 2002), diepoxybutane (Adler et al, 1995), ethylene oxide (Generoso et al, 1986, 1990), ethyl methanesulphonate (Cattanach et al, 1968; Ehling et al, 1968), ethyl nitrosourea (Generoso et al, 1984), etoposide (Bishop et al, 1997), glycidamide (Generoso et al, 1996), isopropyl methanesulfonate (Ehling and Neuhäuser‐Klaus, 1995; Generoso et al, 1979a), melphalan (Generoso et al, 1995), 6‐mercaptopurine (Generoso et al, 1975), methyl methanesulfonate (Lang and Adler, 1977), methyl nitrosourea (Generoso et al, 1984), mitomycin C (Ehling, 1971; Adler, 1980), procarbazine (Ehling, 1974; Adler, 1980), triethylenemelamine (Cattanach, 1957; Bateman, 1960), trophosphamide (Adler et al, 1994b; Ehling and Neuhäuser‐Klaus, 1994), and X‐rays (Ehling, 1971; Searle et al, 1974).…”

Section: Methods For Investigating Paternally‐transmitted Chromosomalmentioning

confidence: 99%

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Marchetti

Wyrobek

2005

Birth Defects Research Pt C

121

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Paternally transmitted chromosomal damage has been associated with pregnancy loss, developmental and morphological defects, infant mortality, infertility, and genetic diseases in the offspring including cancer. There is epidemiological evidence linking paternal exposure to occupational or environmental agents with an increased risk of abnormal reproductive outcomes.There is also a large body of literature on germ cell mutagenesis in rodents showing that treatment of male germ cells with mutagens has dramatic consequences on reproduction producing effects such as those observed in human epidemiological studies. However, we know very little about the etiology, transmission and early embryonic consequences of paternallyderived chromosomal abnormalities. The available evidence suggests that: 1) there are distinct patterns of germ cell-stage differences in the sensitivity of induction of transmissible genetic damage with male postmeiotic cells being the most sensitive; 2) cytogenetic abnormalities at first metaphase after fertilization are critical intermediates between paternal exposure and abnormal reproductive outcomes; and, 3) there are maternally susceptibility factors that may have profound effects on the amount of sperm DNA damage that is converted into chromosomal aberrations in the zygote and directly affect the risk for abnormal reproductive outcomes.

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Section: Methods For Investigating Paternally‐transmitted Chromosomalmentioning

confidence: 99%

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Marchetti

Wyrobek

2005

Birth Defects Research Pt C

121

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“…For example, butadiene was genotoxic in germ cells of male mice in multiple assays, while results in the single dominant lethal study in rats were negative (Morrissey et al, 1990;Anderson et al, 1993;Adler et al, 1994Adler et al, , 1995aAdler et al, , 1998Xiao & Tates, 1995;BIBRA International, 1996a, 1996bBrinkworth et al, 1998;Pacchierotti et al, 1998;Tommasi et al, 1998). Other effects on germ cells in mice have been reported, including an increased incidence of chromosomal aberrations in zygotes produced by exposed males, heritable translocations, sperm head abnormalities, micronuclei in spermatids, and DNA damage (Morrissey et al, 1990;Adler et al, 1995aAdler et al, , 1998Xiao & Tates, 1995;Brinkworth et al, 1998;Pacchierotti et al, 1998;Tommasi et al, 1998); however, these endpoints have not been investigated in rats. With respect to effects on somatic cells, although butadiene was mutagenic at the hprt locus in both mice and rats (Cochrane & Skopek, 1993, 1994Tates et al, 1994Tates et al, , 1998Meng et al, 1998Meng et al, , 2000, its mutagenic potency was greater in mice (Meng et al, 1998(Meng et al, , 2000.…”

Section: Carcinogenicity and Genotoxicitymentioning

confidence: 99%

1,3-Butadiene: Exposure Estimation, Hazard Characterization, and Exposure-Response Analysis

Hughes

Walker

et al. 2003

Journal of Toxicology and Environmental Health, Part B

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1,3-Butadiene has been assessed as a Priority Substance under the Canadian Environmental Protection Act. The general population in Canada is exposed to 1,3-butadiene primarily through ambient air. Inhaled 1,3-butadiene is carcinogenic in both mice and rats, inducing tumors at multiple sites at all concentrations tested in all identified studies. In addition, 1,3-butadiene is genotoxic in both somatic and germ cells of rodents. It also induces adverse effects in the reproductive organs of female mice at relatively low concentrations. The greater sensitivity in mice than in rats to induction of these effects by 1,3-butadiene is likely related to species differences in metabolism to active epoxide metabolites. Exposure to 1,3-butadiene in the occupational environment has been associated with the induction of leukemia; there is also some limited evidence that 1,3-butadiene is genotoxic in exposed workers. Therefore, in view of the weight of evidence of available epidemiological and toxicological data, 1,3-butadiene is considered highly likely to be carcinogenic, and likely to be genotoxic, in humans. Estimates of the potency of butadiene to induce cancer have been derived on the basis of both epidemiological investigation and bioassays in mice and rats. Potencies to induce ovarian effects have been estimated on the basis of studies in mice. Uncertainties have been delineated, and, while there are clear species differences in metabolism, estimates of potency to induce effects are considered justifiably conservative in view of the likely variability in metabolism across the population related to genetic polymorphism for enzymes for the critical metabolic pathway.

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“…Clastogenicity data in somatic and germinal cells of mice and in somatic cells of exposed workers were subjected to the parallelogram approach for human risk assessment proposed by Sobels (1989). Dose–response data were available for clastogenicity of butadiene in somatic and in germinal cells from the mouse bone marrow micronucleus test and the heritable translocation assay ( Adler et al ., 1994 , 1998). For both end‐points the dose–response relationships were linear which allowed the calculation of doubling doses.…”

Section: Genetic Risk Estimatesmentioning

confidence: 99%

Spermatogenesis and mutagenicity of environmental hazards: extrapolation of genetic risk from mouse to man

Adler

2000

Andrologia

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To perform germ cell mutagenicity studies it is mandatory to know the duration of the different stages of spermatogenesis. The timing of male germ cell development determines the test protocols. Chemical mutagens are characterized by their differential spermatogenic responses, e.g. different chemicals induce mutations in different germ cell stages. Knowledge of the sensitive germ cell stages for a test agent is essential for the evaluation of the genetic hazard, i.e. stem cell effects present permanent genetic hazards and post-stem cell effects present transient hazards. A variety of assays are available to determine germ cell mutagenicity in treated animals or in the progeny of treated animals. Germ cell cytogenetics in differentiating spermatogonia and the dominant lethal assay are used for genetic hazard identification. Their results allow categorization of chemicals as germ cell mutagens (Maximale Arbeitsplatz Konzentration categories for germ cell mutagens). Gene mutations or reciprocal chromosome translocations induced in germ cells are assessed by observation of mutant offspring of treated males. These results are applicable to the quantification of genetic hazards for chemical exposures which cannot be avoided, i.e. for occupational exposures to chemicals such as butadiene.

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Dose response study for 1,3-butadiene-induced dominant lethal mutations and heritable translocations in germs cells of male mice

Cited by 18 publications

References 17 publications

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

Mechanisms and consequences of paternally‐transmitted chromosomal abnormalities

1,3-Butadiene: Exposure Estimation, Hazard Characterization, and Exposure-Response Analysis

Spermatogenesis and mutagenicity of environmental hazards: extrapolation of genetic risk from mouse to man

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