Measurement of plasma or urinary metabolites and Hprt mutant frequencies following inhalation exposure of mice and rats to 3-butene-1,2-diol

Walker, Dale M.; McDonald, Jacob D.; Meng, Quanxin; Kracko, Dean; Bauer, Michael J.; Seilkop, Steven K.; Walker, Elizabeth L.; Henderson, Rogene F.; Walker, Vernon E.

doi:10.1016/j.cbi.2007.01.017

Cited by 2 publications

(1 citation statement)

References 33 publications

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“…Current assays for mutagen detection comprise a range of test systems including bacteria [Ames assay; Ames et al, 1975; Gatehouse et al ., 1994], cultured cells from various species [thymidine kinase gene assays; Moore et al , 1985, 2005] and whole animal models utilizing both nontransgenic [Walker et al , 2007] as well as specialized transgenic rodents [Big Blue ® , Muta™Mouse; Morrison and Ashby, 1994; Nohmi et al , 2000]. One more recent method that has gained considerable attention within the last decade is based on the phosphatidylinositol glycan complement class A ( Pig-a ) gene.…”

Section: Introductionmentioning

confidence: 99%

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk^+/− cells and the CD90.2 antigen

Bemis

Avlasevich

Labash

et al. 2017

Environ and Mol Mutagen

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Lack of cell surface glycosylphosphatidylinositol (GPI)-anchored protein(s) has been used as a reporter of Pig-a gene mutation in several model systems. As an extension of this work, our laboratory initiated development of an in vitro mutation assay based on the flow cytometric assessment of CD90.2 expression on the cell surface of the mouse lymphoma cell line L5178Y/Tk 1/2 . Cells were exposed to mutagenic and nonmutagenic compounds for 24 hr followed by washout and incubation for an additional 7 days. Following this mutant manifestation time, cells were labeled with fluorescent antibodies against CD90.2 and CD45 antigens. These reagents indicated the presence of GPI-anchored proteins and general cell surface membrane receptor integrity, respectively. Instrument set-up was aided by parallel processing of a GPI anchordeficient subclone. Results show that the mutagens reproducibly caused increased frequencies of mutant phenotype cells, while the nonmutagens did not. Further modifications to the method, including application of a viability dye and an isotype control for instrument set-up, were investigated. As a means to verify that the GPI-anchored protein-negative phenotype reflects bona fide Pig-a gene mutation, sequencing was performed on 38 CD90.2-negative L5178Y/Tk 1/2 clones derived from cultures treated with ethyl methanesulfonate. All clones were found to have mutation(s) within the Pig-a gene. The continued investigation of L5178Y/Tk 1/2 cells, CD90.2 labeling, and flow cytometric analysis as the basis of an in vitro mutation assay is clearly supported by this work. These data also provide evidence of the reliability of using GPI anchor-deficiency as a valid reporter of Pig-a gene mutation. Environ. Mol. Mutagen. 59:18-29, 2018. V C 2017 Wiley Periodicals, Inc.

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Section: Introductionmentioning

confidence: 99%

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk^+/− cells and the CD90.2 antigen

Bemis

Avlasevich

Labash

et al. 2017

Environ and Mol Mutagen

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International Symposium on the Evaluation of Butadiene and Chloroprene Health Risks

Himmelstein

Baan

Albertini

et al. 2007

Chemico-Biological Interactions

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Measurement of plasma or urinary metabolites and Hprt mutant frequencies following inhalation exposure of mice and rats to 3-butene-1,2-diol

Cited by 2 publications

References 33 publications

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk^+/− cells and the CD90.2 antigen

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk^+/− cells and the CD90.2 antigen

International Symposium on the Evaluation of Butadiene and Chloroprene Health Risks

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Measurement of plasma or urinary metabolites and Hprt mutant frequencies following inhalation exposure of mice and rats to 3-butene-1,2-diol

Cited by 2 publications

References 33 publications

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk+/− cells and the CD90.2 antigen

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk+/− cells and the CD90.2 antigen

International Symposium on the Evaluation of Butadiene and Chloroprene Health Risks

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Product

Resources

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Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk^+/− cells and the CD90.2 antigen

Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig‐a gene Mutation: Support from an in vitro assay based on L5178Y/Tk^+/− cells and the CD90.2 antigen