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Results for “Acrylates”

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At least 19 recordsLinked to original sources
PubMed1988

Genotoxicity of acrylic acid, methyl acrylate, ethyl acrylate, methyl methacrylate, and ethyl methacrylate in L5178Y mouse lymphoma cells.

A series of monomeric acrylate/methacrylate esters (methyl acrylate, ethyl acrylate, methyl methacrylate, and ethyl methacrylate) as well as acrylic acid were examined for genotoxic activity in L5178Y mouse lymphoma cells without exogenous activation. All five compounds induced concentration-dependent increases in mutant frequency. Small-colony, trifluorothymidine-resistant mutants were primarily induced, which suggests that these compounds may act via a clastogenic mechanism. This prediction was confirmed by the finding that all five compounds produced gross chromosome aberrations in mouse lymphoma cells. The two acrylates were much more potent in their response than acrylic acid. Methyl acrylate (22 micrograms/ml, survival = 18%) induced 385 mutants/10(6) survivors (total mutant frequency less the spontaneous mutant frequency) and 45 chromosome aberrations/100 cells analyzed (total aberrations less the spontaneous background). Ethyl acrylate (37.5 micrograms/ml, survival = 15%) induced 683 mutants/10(6) survivors and 48 aberrations/50 cells analyzed. Acrylic acid (500 micrograms/ml, survival = 22%) induced 245 mutants/10(6) survivors and 37 aberrations/100 cells analyzed. The two methacrylates required higher concentrations to induce a positive response. Methyl methacrylate (2,799 micrograms/ml, survival = 11%) induced 230 mutants/10(6) survivors and 29 aberrations/200 cells analyzed. Ethyl methacrylate was extremely difficult to test because of a plateau in the dose response, over which the toxicity fluctuated from 2% to 37% survival. Positive responses (twice the spontaneous background) were only obtained at toxicity levels with less than approximately 20% survival. A concentration of 1,626 micrograms/ml (survival = 16%) induced 83 mutants/10(6) survivors and 11 aberrations/200 cells analyzed. The evidence suggests that the genotoxicity of these compounds is most likely due to a clastogenic mechanism.

Acrylates↗
PubMed1985

Dermal oncogenicity bioassays of monofunctional and multifunctional acrylates and acrylate-based oligomers.

Several important components of photocurable coatings were studied for dermal tumorigenic activity by repeated application to the skin of mice. The substances tested were 2-ethylhexyl acrylate (EHA) and methylcarbamoyloxyethyl acrylate (MCEA) (monomers); neopentyl glycol diacrylate (NPGDA), esterdiol-204-diacrylate (EDDA), and pentaerythritol tri(tetra)acrylate (PETA) (cross-linkers); and three acrylated urethane oligomers. For each bioassay, 40 C3H/HeJ male mice were dosed 3 times weekly on the dorsal skin for their lifetime with the highest dose of the test agent that caused no local irritation or reduction in body weight gain. Two negative control groups received acetone (diluent) only. A positive control group received 0.2% methylcholanthrene (MC). NPGDA and EHA had significant tumorigenic activity with tumor yields of eight and six tumor-bearing mice (three and two malignancies), respectively. The MC group had 34 mice with carcinomas and 1 additional mouse with a papilloma. MCEA had no dermal tumorigenic activity but resulted in early mortality. No skin tumors in the treatment area were observed in the other groups. Additional studies will be necessary to elucidate possible relationships between structure and tumorigenic activity for the acrylates.

Acrylates↗
PubMed1989

Allergic contact dermatitis from dental composite resins due to aromatic epoxy acrylates and aliphatic acrylates.

7 patients were occupationally sensitized to dental composite resin products (DCR): 6 dental nurses and 1 dentist. All had a positive patch test to their DCR. 2 independent types of allergy were seen; (a) aromatic epoxy acrylate, and/or (b) aliphatic acrylates. 4 out of 5 patients reacted to BIS-GMA, the most widely used aromatic epoxy acrylate in DCR, but not the dentist. She and 2 dental nurses were allergic to aliphatic acrylates, including triethylene glycol dimethacrylate (TREGDMA) and triethylene diglycol diacrylate (TREGDA). 4 patients were allergic to epoxy resin (ER) (containing mainly MW 340), possibly an impurity in some DCR. 2 patients were also allergic to methyl methacrylate (MMA): the dentist, had been exposed to MMA, but the nurse's exposure was uncertain. 1 patient was also allergic to rubber gloves, 2 to rubber chemicals but not their gloves, and 5 to disinfectants used. diagnosis was delayed as long as 13 years in spite of previous patch testing. Dermatologists need to use the patients' own DCR and the (meth)acrylate series for patch testing. No dental nurses could continue their occupation, but the dentist could occasionally handle DCR if wearing PVC gloves. Dental personnel need to know about the risks of DCR, and use no-touch techniques and protective gloves.

Acrylic Resins↗
PubMed1989

Non-genotoxicity of acrylic acid and n-butyl acrylate in a mammalian cell system (SHE cells).

Acrylic acid (AA), ethyl acrylate (EA) and n-butyl acrylate (BA) are widely used in the production of plastics, coatings and acrylic fibres. Occupational exposure occurs primarily via inhalation and/or skin contact. In chronic inhalation experiments EA and BA did not induce neoplastic changes in rats and mice (Klimisch and Reininghaus 1984; Miller et al. 1985). Additional investigations showed that AA and BA were not carcinogenic in mice after chronic dermal application (De Pass et al. 1984). However, recently other authors reported a weak carcinogenic potential of AA and BA after chronic dermal administration to mice (Cote et al. 1986). The conditions of the latter study lead to the suggestion that the observed tumours had developed secondarily due to the local irritating and corrosive properties of AA and BA. This view is supported by the negative results of AA, EA and BA in the conventional Ames test (Waegemaekers and Bensink 1984). Mutagenicity data in mammalian cell systems of EA were equivocal (Henschler 1986) and were lacking for AA and BA. For this reason the mutagenic potential of AA and BA was investigated in Syrian hamster embryo fibroblasts (SHE cells). DNA repair (UDS assay), chromosomal changes (micronucleus assay) and morphological transformation were chosen as biological end-points.

Acrylates↗
PubMed1987

The disposition and metabolism of acrylic acid and ethyl acrylate in male Sprague-Dawley rats.

Following oral dosing of [2,3-14C]acrylic acid (AA; 4, 40, or 400 mg/kg) and [2,3-14C]ethyl acrylate (EA; 2, 20, or 200 mg/kg), the dosed radioactivity was rapidly excreted, with 50-75% of the dose for both compounds eliminated within 24 hr. The primary excretory metabolite for both compounds is carbon dioxide, accounting for 44-68% of the dose. HPLC analysis of the urine of AA- and EA-dosed animals indicated the presence of 3-hydroxypropionic acid. The detection of this metabolite suggests the incorporation of AA into propionic acid metabolism and may explain the rapid evolution of carbon dioxide from AA and EA. HPLC analysis of urine from EA-dosed rats revealed the presence of two metabolites derived from glutathione conjugation, N-acetyl-S-(carboxyethyl)cysteine and N-acetyl-S-(carboxyethyl)cysteine ethyl ester. The excretion of the N-acetyl cysteine derivatives of EA, expressed as a percentage of the dosed compound, decreased in a dose-dependent manner that may be attributed to the depletion of glutathione in organs primarily responsible for glutathione conjugation. No significant decrease in hepatic nonprotein sulfhydryl (NPSH) content was observed following oral dosing with EA at 2-200 mg/kg. However, the depletion of NPSH content at the dosing site, forestomach, and glandular stomach, decreased significantly between 0.02 and 0.2% EA in the dose solution (2 and 20 mg/kg). This observation would suggest that the dosing site represents a significant site of conjugation for relatively low doses of EA. Treatment with the carboxylesterase inhibitor, tri-o-cresyl phosphate (TOCP), 18 hr prior to acrylate dosing potentiated the depletion of hepatic nonprotein sulfhydryls, emphasizing the dominance of hydrolysis as a systemic detoxifying mode in this species. In contrast to EA, AA did not significantly decrease NPSH content in the liver, blood, or forestomach at oral doses of less than 8% AA in the dose solution (400 mg/kg), although a significant depletion of NPSH was observed in the glandular stomach at doses greater than 0.08% (4 mg/kg). No conjugation involving the double bond of AA could be detected in in vitro reactions with glutathione or in the in vivo metabolites, suggesting a secondary effect of AA on NPSH content in these organs. The weights of the forestomach and glandular stomach increased with AA dose, reflecting gross edema and inflammation. With EA this effect on organ weight was only demonstrated in the forestomach, and the response was increased when hydrolysis of EA was inhibited with TOCP.(ABSTRACT TRUNCATED AT 400 WORDS)

Acrylates↗
PubMed1991

Chronic toxicity and oncogenicity of inhaled methyl acrylate and n-butyl acrylate in Sprague-Dawley rats.

No exposure-related clinical signs or lesions of systemic toxicity and no oncogenic responses were observed in male and female Sprague-Dawley rats exposed by inhalation to methyl acrylate (MA) or n-butyl acrylate (BA) vapours, at concentrations of 0, 15, 45 and 135 ppm. The rats were whole-body-exposed 6 hr/day, 5 days/wk, for 24 consecutive months. There was a 6-month post-exposure observation period for subgroups of BA-exposed rats. Atrophy of the neurogenic epithelial cells and hyperplasia of reserve cells were observed in the nasal mucosa of all MA- and BA-exposed groups. These changes were dose related and mainly affected the anterior part of the olfactory epithelium. Opacity and neovascularization of the cornea were seen in all MA-exposed groups and in the group exposed to 135 ppm BA. These toxic effects of the olfactory epithelium and cornea were attributed to the known irritancy of MA and BA. In the BA subgroups kept for a 6-month post-exposure observation, reconstructive effects, such as replacement of altered olfactory epithelium with respiratory epithelium, and partial regression of corneal neovascularization were observed.

Acrylates↗
PubMed1989

Modeling the reactivity of acrylic acid and acrylate anion with biological nucleophiles.

Based on the results of prior in-vitro reactivity experiments, the pathway for the Michael addition of two representative nucleophiles (methylamine and imidazole) to acrylate anion (AA-) was explored with the semiempirical quantum model, AM1. The results of the calculations indicate that there is no viable reaction pathway for the addition of nucleophiles to AA-. An alternative route for the formation of the Michael products via the non-ionized form of acrylic acid (AA) was explored and found to be theoretically possible. The alternative route is plausible, but is considered to be insignificant in vivo based upon the rapid metabolism and excretion of AA (excretion half-life of 1-8 h after oral dosing).

Acrylates↗
PubMed1987

The isolation and characterization of 2-carboxyethyl adducts following in vitro reaction of acrylic acid with calf thymus DNA and bioassay of acrylic acid in female Hsd:(ICR)Br mice.

Reaction of acrylic acid (AA) at pH 7.0 and 37 degrees C for 40 days with 2'-deoxyadenosine (dAdo), 2'-deoxycytidine (dCyd), 2'-deoxyguanosine (dGuo) and thymidine (dThd) resulted in the formation of 2-carboxyethyl (CE) adducts via Michael addition. The alkylated 2'-deoxynucleoside adducts isolated (percent yield after 40 days) were 1-CE-dAdo (5%), N6-CE-dAdo (11%) (via Dimroth rearrangement of 1-CE-dAdo), 3-CE-dCyd (7.5%), 7-CE-Gua (4%), 7,9-bis-CE-Gua (0.9%) (formed by reaction of AA with depurinated 7-CE-Gua during the course of the reaction) and 3-CE-dThd (0.5%). The products isolated following in vitro reaction of AA with calf thymus DNA at pH 7.0 and 37 degrees C for 40 days were (nmol/mg DNA) 1-CE-Ade (9.9), N6-CE-Ade (8.2), 7-CE-Gua (7.2) and 3-CE-Thy (1.9). Compound 3-CE-Cyt was not detected. Thus the adducts formed following in vitro reaction of AA with DNA are identical to those formed by in vitro reaction of the carcinogen beta-propiolactone (BPL) with DNA as reported in an earlier paper. Structures were assigned on the basis of identical UV spectra, Rf values on paper chromatograms and Rt values on HPLC as marker compounds prepared from reactions of BPL with 2'-deoxynucleosides and 2'-deoxynucleotides-5'-monophosphoric acids. AA was assayed for carcinogenic activity by s.c. injection (20 mumol, once a week for 52 weeks) in female Hsd: (ICR)Br mice. Two mice with sarcomas at the site of application were observed out of 30 mice. Malignancies were not observed in solvent and no-treatment controls. The bioassay results reported in this paper and elsewhere in the same strain of mice suggest that AA is a weak carcinogen in female Hsd:(ICR)Br mice.

Acrylates↗