Analysis of the genotoxicity of nine acrylate/methacrylate compounds in L5178Y mouse lymphoma cells. 1989

K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
Health Effects Division, US Environmental Protection Agency, Washington, DC 20460.

Nine acrylate/methacrylate esters were tested for the induction of mutations, aberrations and micronuclei in cultured L5178Y mouse lymphoma cells without exogenous activation. With the exception of 2-ethylhexyl acrylate, and dicyclopentenyloxyethyl methacrylate which produced equivocal mutagenic responses, the other seven compounds (2-hydroxyethyl acrylate, dicyclopentenyloxyethyl acrylate, tetraethylene glycol diacrylate, tetraethylene glycol dimethacrylate, trimethylolpropane triacrylate, trimethylolpropane trimethacrylate, and pentaerythritol triacrylate) produced positive mutagenic responses with different potencies. For the mutagenic acrylates/methacrylates, primarily small-colony, trifluorothymidine (TFT)-resistant mutants were induced, suggesting a clastogenic mechanism that was supported by increased aberrations and micronucleus frequencies (except for trimethylolpropane trimethacrylate which was positive for aberration but not micronucleus induction). Generally, it was found that multifunctional compounds (esters with greater than 1 functional vinyl group) required lower concentrations than monofunctional compounds to induce maximal cytotoxic, mutagenic, and clastogenic responses. In addition, acrylates were generally more potent than their corresponding methacrylates. This information and these comparative activities will provide some guidance for setting priorities of concern for hazard consideration for acrylate/methacrylate ester compounds.

UI MeSH Term Description Entries
D007940 Leukemia L5178 An experimental lymphocytic leukemia of mice. Lymphoma L5178,L5178, Leukemia,L5178, Lymphoma
D008689 Methacrylates Acrylic acids or acrylates which are substituted in the C-2 position with a methyl group. Methacrylate
D009153 Mutagens Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. Clastogen,Clastogens,Genotoxin,Genotoxins,Mutagen
D009154 Mutation Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations. Mutations
D002869 Chromosome Aberrations Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS. Autosome Abnormalities,Cytogenetic Aberrations,Abnormalities, Autosome,Abnormalities, Chromosomal,Abnormalities, Chromosome,Chromosomal Aberrations,Chromosome Abnormalities,Cytogenetic Abnormalities,Aberration, Chromosomal,Aberration, Chromosome,Aberration, Cytogenetic,Aberrations, Chromosomal,Aberrations, Chromosome,Aberrations, Cytogenetic,Abnormalities, Cytogenetic,Abnormality, Autosome,Abnormality, Chromosomal,Abnormality, Chromosome,Abnormality, Cytogenetic,Autosome Abnormality,Chromosomal Aberration,Chromosomal Abnormalities,Chromosomal Abnormality,Chromosome Aberration,Chromosome Abnormality,Cytogenetic Aberration,Cytogenetic Abnormality
D002875 Chromosomes In a prokaryotic cell or in the nucleus of a eukaryotic cell, a structure consisting of or containing DNA which carries the genetic information essential to the cell. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed) Chromosome
D004249 DNA Damage Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS. DNA Injury,DNA Lesion,DNA Lesions,Genotoxic Stress,Stress, Genotoxic,Injury, DNA,DNA Injuries
D004305 Dose-Response Relationship, Drug The relationship between the dose of an administered drug and the response of the organism to the drug. Dose Response Relationship, Drug,Dose-Response Relationships, Drug,Drug Dose-Response Relationship,Drug Dose-Response Relationships,Relationship, Drug Dose-Response,Relationships, Drug Dose-Response
D000179 Acrylates Derivatives of acrylic acid (the structural formula CH2
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia

Related Publications

K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
January 1988, Environmental and molecular mutagenesis,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
January 1993, Mutation research,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
January 1999, Environmental and molecular mutagenesis,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
January 2001, Environmental and molecular mutagenesis,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
June 1986, Mutation research,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
January 2005, Environmental and molecular mutagenesis,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
December 1998, Toxicological sciences : an official journal of the Society of Toxicology,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
May 2000, Mutagenesis,
K L Dearfield, and C S Millis, and K Harrington-Brock, and C L Doerr, and M M Moore
May 1988, Mutagenesis,
Copied contents to your clipboard!