Reevaluation of the induction of specific-locus mutations in spermatogonia of the mouse by acrylamide

Ehling, U.H.; Neuhäuser-Klaus, A.

doi:10.1016/0165-7992(92)90106-r

Cited by 48 publications

(19 citation statements)

References 16 publications

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“…spermatids confirms that the major genotoxic effect of The significant increase in the number of zygotes with AA occurs in the postmeiotic stages. Sperm and late sperstructural aberrations found after treatment of pachytene matids were also the most sensitive cells for the induction spermatocytes illustrates the importance of using our of DL [Shelby et al, 1986;Ehling and Neuhäuser-Klaus, PAINT/DAPI analysis, rather than PAINT analysis alone 1992], HT [Shelby et al, 1987;Adler et al, 1994], and as typically performed in somatic studies. Had we used SL [Russell et al, 1991].…”

Section: Discussionmentioning

confidence: 95%

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Induction of chromosomal aberrations in mouse zygotes by acrylamide treatment of male germ cells and their correlation with dominant lethality and heritable translocations

Marchetti¹,

Lowe²,

Bishop³

et al. 1997

Environ. Mol. Mutagen.

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The objectives of this research were: 1) to investigate the time course of the cytogenetic defects induced by acrylamide (AA) treatment (5 × 50 mg/kg) of male germ cells in first‐cleavage zygote metaphases using PAINT/DAPI analysis, and 2) to characterize the correlation between chromosomal aberrations at first cleavage, dominant lethality, and heritable translocations. PAINT/DAPI analysis employs multicolor fluorescence in situ hybridization painting plus DAPI staining to detect both stable and unstable chromosomal aberrations at first‐cleavage metaphase of the zygote. High levels of chromosomally defective zygotes were detected after mating at all postmeiotic stages (20–190‐fold, P < 0.001). Early spermatozoa (6.5 d post‐treatment) were the most sensitive, with 76% of the zygotes carrying cytogenetic defects. A significant 10‐fold increase was also detected 27.5 d post‐treatment, indicating that AA had a cytogenetic effect on meiotic stages. PAINT/DAPI analysis revealed that: 1) AA‐induced chromosomal breaks occurred at random, and 2) the frequencies of symmetrical and asymmetrical exchanges were similar at all mating days, except 9.5 d after AA treatment, where significantly (P < 0.02) more asymmetrical aberrations were found. Furthermore, the proportions of zygotes carrying unstable and stable chromosomal aberrations followed a similar post‐treatment time course as the proportions of dominant lethality among embryos and heritable translocations among offspring. These findings indicate that PAINT/DAPI analysis of zygotic metaphases is a promising method for detecting male germ cell mutagens capable of inducing chromosomal aberrations and for evaluating the associated risks for embryonic loss and balanced translocations at birth. Environ. Mol. Mutagen. 30:410–417, 1997 © 1997 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 95%

“…injection of 7.5 I.U. of pregnant mare's häuser- Klaus, 1992], particularly after treatment of mouse serum (PMS, Sigma Chemical, St. Louis. MO) to increase the number late spermatids and early spermatozoa.…”

Section: Introductionmentioning

confidence: 99%

Induction of chromosomal aberrations in mouse zygotes by acrylamide treatment of male germ cells and their correlation with dominant lethality and heritable translocations

Marchetti¹,

Lowe²,

Bishop³

et al. 1997

Environ. Mol. Mutagen.

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“…A lower frequency of pregnant females obtained after exposure of spermatozoa to AA and X-rays + AA [14] can be compared to a higher frequency of sperm head abnormalities, because malformed spermatozoa are not able to fertilize. Also, the results of other AA studies suggest that the late spermatids and spermatozoa are the most susceptible to damage [13,15,17,[44][45][46] . In previous studies, a significant increase in micronucleus frequency in bone marrow was observed 24 h after treatment with 50-100 mg/kg bw of AA [4,6,7].…”

Section: Discussionmentioning

confidence: 99%

“…Several authors have found positive effects in micronucleus tests in spermatids of rodents [9][10][11][12]. AA causes dominant lethal mutations in mice [8,[13][14][15] and in rats [16,17], and produces increases in malformed sperm heads [18].…”

Section: Introductionmentioning

confidence: 97%

Induction of micronuclei in bone marrow and sperm head abnormalities after combined exposure of mice to low doses of X-rays and acrylamide

Dobrzyńska¹,

Gajewski²

2000

Teratog. Carcinog. Mutagen.

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“…The study confirmed the stage sensitivity of spermatogenesis to AA observed in the earlier dominant lethal studies. While specific locus mutations were observed originally in the same germ cell stages as the dominant lethal mutations (Russell et al, 1991), it was shown later that AA also induced mutations in spermatogonial stem cells of mice (Ehling and Neuhäuser-Klaus, 1992). Originally, alkylation of chromosomal protamines in late spermatids and sperm was assumed to cause the clastogenic effects in male germ cells (Sega et al, 1989).…”

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confidence: 99%

Heritable translocations induced by dermal exposure of male mice to acrylamide

Adler¹,

Gonda²,

Angelis³

et al. 2004

Cytogenet Genome Res

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Acrylamide (AA) is an important industrial chemical used mainly in the production of polymers. It can be absorbed through the skin. AA was shown to be a germ cell clastogen that entails a genetic risk for exposed workers. The genetic risk calculation was based on mouse heritable translocation test data obtained after acute intraperitoneal (ip) exposure (Adler et al., 1994). To obtain a correction factor between ip and dermal exposure, dominant lethal and heritable translocation tests were carried out with dermal exposure of male mice to AA. In the dominant lethal test, male (102/El × C3H/El)F₁ mice were exposed by dermal application to the shaved backs of 50 mg/kg AA per day on five consecutive days or to five daily ip injections of 50 mg/kg AA. One day after the end of exposure, the males were mated to untreated females of the same hybrid stock for four days and females were changed every four days for a total of five matings. Dominant lethal effects were found during matings 1–3. For ip exposure, these values were 81.7, 85.7 and 45.4%, respectively; for dermal exposure the corresponding values were 22.1, 30.6 and 16.5%, respectively. In the heritable translocation assay, male C3H/El mice were treated with five dermal exposures of 50 mg/kg AA and mated 1.5–8.5 days after the end of exposure to untreated female 102/El mice. Pregnant females were allowed to come to term and all offspring were raised to maturity. Translocation carriers among the F₁ progeny were selected by a sequential fertility testing and cytogenetic analysis including G-band karyotyping and M-FISH. A total of 475 offspring were screened and 41 translocation carriers were identified. The observed translocation frequency after dermal exposure was 8.6% as compared to 21.9% after similar ip exposure (Adler, 1990). The calculated ratio of ip vs. dermal exposure of 0.39 can be applied to obtain a more realistic calculation of genetic risk for dermally exposed workers.

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Reevaluation of the induction of specific-locus mutations in spermatogonia of the mouse by acrylamide

Cited by 48 publications

References 16 publications

Induction of chromosomal aberrations in mouse zygotes by acrylamide treatment of male germ cells and their correlation with dominant lethality and heritable translocations

Induction of chromosomal aberrations in mouse zygotes by acrylamide treatment of male germ cells and their correlation with dominant lethality and heritable translocations

Induction of micronuclei in bone marrow and sperm head abnormalities after combined exposure of mice to low doses of X-rays and acrylamide

Heritable translocations induced by dermal exposure of male mice to acrylamide

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