Acrylamide-induced chromosomal damage in male mouse germ cells detected by cytogenetic analysis of one-cell zygotes

Pacchierotti, Francesca; Tiveron, Cecilia; D’Archivio, Massimo; Bassani, B.; Cordelli, Eugenia; Leter, Giorgio; Spanò, Marcello

doi:10.1016/0027-5107(94)90102-3

Cited by 35 publications

(20 citation statements)

References 26 publications

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“…Some environmental mutagens are able to induce aneuploidy [Russo et al, 1984;Miller and Adler, 1992;Leopardi et al, 1993;Allen et al, 1995;Adler et al, 1996] and chromosomal aberrations in reproductive cells [Pacchierotti et al, 1994], e.g., translocations, deletions, or duplications of chromosomal segments. The combination of two multicolor FISH assays described in this article opens the door to future studies on the induction and persistence of numerical and structural chromosomal abnormalities in men exposed to drugs and environmental mutagens.…”

Section: Structural Aberrationsmentioning

confidence: 99%

Numerical and structural chromosomal abnormalities detected in human sperm with a combination of multicolor FISH assays

Baumgartner

Hummelen

Lowe

et al. 1999

Environ. Mol. Mutagen.

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Section: Structural Aberrationsmentioning

confidence: 99%

Numerical and structural chromosomal abnormalities detected in human sperm with a combination of multicolor FISH assays

Baumgartner

Hummelen

Lowe

et al. 1999

Environ. Mol. Mutagen.

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“…An advantage of this system is that the relative contribution of each parent to the incidence of chromosome anomalies can be assessed independently because the paternal and maternal chromosomes remain separated until the metaphase plate of the first mitotic division (McGaughey & Chang 1969), and because the maternal chromosomes show a higher degree of condensation (Donahue 1972). The analysis of mouse zygotes by conventional cytogenetics has already been used to demonstrate the induction of aneuploidy after treatment of female germ cells (reviewed by Mailhes & Marchetti 1994), and the induction of structural aberrations after treatment of male germ cells with various alkylating agents (Tanaka et al 1981, Albanese 1982, Matsuda & Tobari 1988, Pacchierotti et al 1994, radiomimetics or irradiation . Consistent findings of the male exposure studies were: (1) post-meiotic effects were primarily observed; and (2) the majority of the aberrations were of the chromosome type, rather than chromatid type, even after treatment with S-phase-dependent chemicals.…”

Section: Introductionmentioning

confidence: 99%

“…The procedure is applied in this study to 1-C1 zygote metaphases collected after post-meiotic treatment of male germ cells with the model germ cell clastogen acrylamide (AA) (Pacchierotti et al 1994). The objectives of our study were to: (1) evaluate the sensitivity of chromosome painting analysis for detecting chromosome aberrations by comparing and contrasting the frequencies and types of chromosome aberrations detected by PAINT analysis and DAPI staining; (2) compare the frequencies of stable and unstable aberrations; and (3) determine whether paternally transmitted chromosome breaks occur at random.…”

Section: Introductionmentioning

confidence: 99%

Paternally inherited chromosomal structural aberrations detected in mouse first-cleavage zygote metaphases by multicolour fluorescencein situ hybridization painting

et al. 1996

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We describe a fluorescence in situ hybridization (FISH) procedure for assessing zygotic risk of paternal exposure to endogenous or exogenous agents. The procedure employs multicolour FISH with chromosome-specific DNA painting probes plus DAPI staining for detecting both balanced and unbalanced chromosomal aberrations in mouse first-cleavage (1-Cl) zygote metaphases. Four composite probes specific for chromosomes 1, 2, 3 or X, each labelled with biotin, plus a composite probe specific for chromosome Y labelled with digoxigenin, were used. We applied this method to evaluate the effects of paternal exposure to acrylamide, a model germ cell clastogen. First-cleavage zygote metaphases, collected from untreated females mated to males whose sperm or late spermatids were treated with acrylamide, were scored for the induction of structural aberrations using both chromosome painting (PAINT analysis) and DAPI analysis. Structural chromosomal aberrations were observed in the sperm-derived, but not in the egg-derived, pronuclei. While 59.4% of the zygotes had structural aberrations by DAPI analysis, 94.1% of the same zygotes had structural aberrations by PAINT analysis (P < 0.001), illustrating the increased sensitivity for detecting translocations and insertions obtained by adding chromosome painting. These findings show that FISH painting of mouse 1-Cl zygotes when used in conjunction with DAPI analysis is a powerful model for investigating the cytogenetic defects transmitted from father to offspring.

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“…or with five daily injections of 50 mg/kg b.w. resulted in significant increases of structural chromosomal aberrations in late spermatids/spermatozoa (Pacchierotti et al, 1994).…”

Section: Mode Of Action Of Thyroid Toxicitymentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

337

170

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EFSA was asked to deliver a scientific opinion on acrylamide (AA) in food. AA has widespread uses as an industrial chemical. It is also formed when certain foods are prepared at temperatures above 120 °C and low moisture, especially in foods containing asparagine and reducing sugars. The CONTAM Panel evaluated 43 419 analytical results from food commodities. AA was found at the highest levels in solid coffee substitutes and coffee, and in potato fried products. Mean and 95th percentile dietary AA exposures across surveys and age groups were estimated at 0.4 to 1.9 µg/kg body weight (b.w.) per day and 0.6 to 3.4 µg/kg b.w. per day, respectively. The main contributor to total dietary exposure was generally the category 'Potato fried products (except potato crisps and snacks)'. Preferences in home-cooking can have a substantial impact on human dietary AA exposure. Upon oral intake, AA is absorbed from the gastrointestinal tract and distributed to all organs. AA is extensively metabolised, mostly by conjugation with glutathione but also by epoxidation to glycidamide (GA). Formation of GA is considered to represent the route underlying the genotoxicity and carcinogenicity of AA. Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity were identified as possible critical endpoints for AA toxicity from experimental animal studies. The data from human studies were inadequate for dose-response assessment. The CONTAM Panel selected BMDL 10 values of 0.43 mg/kg b.w. per day for peripheral neuropathy in rats and of 0.17 mg/kg b.w. per day for neoplastic effects in mice. The Panel concluded that the current levels of dietary exposure to AA are not of concern with respect to non-neoplastic effects. However, although the epidemiological associations have not demonstrated AA to be a human carcinogen, the margins of exposure (MOEs) indicate a concern for neoplastic effects based on animal evidence. © European Food SUMMARYFollowing a request from the European Commission, the Panel on Contaminants in the Food Chain (CONTAM Panel) was asked to deliver a scientific opinion on acrylamide (AA) in food. The Panel developed the draft scientific opinion which underwent a public consultation from 1 July 2014 to 15 September 2014. The comments received and how they were taken into account when finalising the scientific opinion were published in an EFSA Technical Report (EFSA, 2015).AA is a low molecular weight, highly water soluble, organic compound. It is used inter alia as an industrial chemical and in the production of polyacrylamides. Heightened concerns about exposure to AA arose in 2002 when it was discovered that it forms when certain foods are prepared at temperatures usually above 120 °C and low moisture. It forms, at least in part, due to a Maillard reaction between certain amino acids, such as asparagine, and reducing sugars. However, several other pathways and precursors have also been proposed to contribute to AA formation. AA forms in numerous baked or fried carbohydrate-rich f...

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Acrylamide-induced chromosomal damage in male mouse germ cells detected by cytogenetic analysis of one-cell zygotes

Cited by 35 publications

References 26 publications

Numerical and structural chromosomal abnormalities detected in human sperm with a combination of multicolor FISH assays

Numerical and structural chromosomal abnormalities detected in human sperm with a combination of multicolor FISH assays

Paternally inherited chromosomal structural aberrations detected in mouse first-cleavage zygote metaphases by multicolour fluorescencein situ hybridization painting

Scientific Opinion on acrylamide in food

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