Genotoxic effects of ethyl acrylate and methyl acrylate in the mouse evaluated by the micronucleus test

Przybojewska, Barbara; Dziubałtowska, Elżbieta; Kowalski, Zbigniew W.

doi:10.1016/0165-1218(84)90120-4

Cited by 51 publications

(15 citation statements)

References 4 publications

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“…Progression to neoplasia was also seen in rats treated for 12 mo and allowed a 9-mo recovery, as evident from the presence offorestomach squamous cell papillomas and carcinomas. (6,33) in organs such as the forestomach (13,17), liver (20), upper respiratory tract (25), kidney (31), and urinary bladder (5,7 (3,30). In studies with the L5178Y mouse lymphoma cell system (26).…”

Section: Resultsmentioning

confidence: 99%

Demonstration of a Temporal Relationship Between Ethyl Acrylate-Induced Forestomach Cell Proliferation and Carcinogenicity

et al. 1994

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Section: Resultsmentioning

confidence: 99%

Demonstration of a Temporal Relationship Between Ethyl Acrylate-Induced Forestomach Cell Proliferation and Carcinogenicity

et al. 1994

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“…Mutagenicity studies in several Salmonella typhimiiriiun strains and Drosophila indicated that EA is nonmutagenic with or without the addition of metabolic activation systems (24,33). In contrast, EA was positive in the mouse when evaluated by the micronucleus test (26), a finding which has been disputed by others (1).…”

Section: Introductionmentioning

confidence: 45%

Sustainability of Forestomach Hyperplasia in Rats Treated with Ethyl Acrylate for 13 Weeks and Regression after Cessation of Dosing

1991

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In a chronic study conducted by the National Toxicology Program (NTP), gavage administration of 100 or 200 mg ethyl acrylate (EA)/kg/day, 5 daydweek, to F344 rats and B6C3F1 mice resulted in a significant dose-dependent increase in the incidence of squamous cell papillomas and carcinomas of the forestomach of both sexes of rats and mice. No increase in the incidence of tumors was observed at any other site in these rats. Chemically-induced cell proliferation is currently thought to play a role in the development and progression of chemically-induced neoplasia. Therefore, a stop-study was initiated where 100 or 200 mg EA/ kg (in corn oil) was administered daily, 5 daysiweek, for 13 weeks. Rats sacrificed at the end of the treatment regimen had severe epithelial hyperplasia of the forestomach. No lesions were observed in the glandular stomach or liver of EA-treated rats. Forestomach hyperplasia induced by EA included upward and downward cell proliferation. However, forestomachs of rats treated for 13 weeks and sacrificed 8 weeks after the last EA dose exhibited a significant decline in the incidence and seventy of forestomach mucosal hyperplasia. Histopathologic evaluation of forestomachs of EA-treated rats (13 weeks) which were allowed a 19-monthrecovery (with no exposure to EA) showed further decline in the incidence and severity of mucosal cell hyperplasia. These results indicate that gavage administration of EA to rats results in extensive and sustained forestomach mucosal hyperplasia. The sustainability of forestomach hyperplasia is apparently dependent on the continued exposure of rats to ethyl acrylate, and regressed after cessation of dosing. Furthermore, although enough post-treatment time was allowed for tumors to develop after cessation of EA administration, forestomachs exhibited a nearly complete recovery with no increased incidence of papillomas or carcinomas. It, therefore, remains to be determined what duration of exposure or other factors are critical for reversibility or progression of EA-induced forestomach mucosal hyperplasia to neoplasia.

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“…EA was negative in most mutagenicity assays with and without metabolic activation, as indicated by testing in several Salmonella typhimurium strains and in Drosophila (7). However, EA was positive in one micronucleus mutagenicity study in mice (8), a finding that was later disputed by Ashby et al (9).…”

Section: Introductionmentioning

confidence: 72%

Relationship between the time of sustained ethyl acrylate forestomach hyperplasia and carcinogenicity.

Ghanayem

Sanchez

Maronpot

et al. 1993

Environ Health Perspect

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Chronic administration of ethyl acrylate (EA) by gavage at 100 or 200 mg/kg/day resulted in a significant dose-dependent increase in the incidence of forestomach (FS) squamous cell papiflomas and carcinomas in both sexes of F344 rats and B6C3F, mice. Subsequent work in this laboratory was designed to investigate the relationship between EA-induced FS hyperplasia and carcinogenicity. Current studies have focused on determining the time required for sustained FS hyperplasia to produce neoplastic transformation. Results of these studies demonstrated that gavage administration of EA to male F344 rats at 200 mg/kg/day for 6 or 12 months caused a sustained increase in FS epithelial hyperplasia for as long as exposure to EA continued. However, FS hyperplasia regressed, and no neoplasms developed when animals receiving EA for 6 months were allowed to recover until they were sacrificed at 24 months of age. In contrast, rats treated for 12 months and allowed 9 months recovery developed FS squamous cell carcinomas (3/13) and papillomas (1/13) for a combined incidence of 4/13. No gross lesions were detected in the liver of any of the rats treated with EA or corn oil vehicle, confirming the tissue specificity in the relationship between EA-induced FS hyperplasia and carcinogenesis. In conclusion, the present work has demonstrated that FS hyperplasia is selectively sustained at the site of EA-induced carcinogenicity for as long as EA is administered and has also demonstrated a temporal relationship between FS mucosal hyperplasia and the development of FS neoplasia by EA. It is speculated that whereas a temporal relationship probably exists between FS hyperplasia and tumor development for many chemicals known to increase cell proliferation, this relationship may vary significantly from one chemical to another and with the target tissue and may be influenced by the mutagenicity of chemicals.

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Genotoxic effects of ethyl acrylate and methyl acrylate in the mouse evaluated by the micronucleus test

Cited by 51 publications

References 4 publications

Demonstration of a Temporal Relationship Between Ethyl Acrylate-Induced Forestomach Cell Proliferation and Carcinogenicity

Demonstration of a Temporal Relationship Between Ethyl Acrylate-Induced Forestomach Cell Proliferation and Carcinogenicity

Sustainability of Forestomach Hyperplasia in Rats Treated with Ethyl Acrylate for 13 Weeks and Regression after Cessation of Dosing

Relationship between the time of sustained ethyl acrylate forestomach hyperplasia and carcinogenicity.

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