ArticleChemical research in toxicology2006
Photomutagenicity of anhydroretinol and 5,6-epoxyretinyl palmitate in mouse lymphoma cells.
Article in Chemical research in toxicology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- High-Throughput Testing for Unknown Mutagens and Cytotoxica via Duplex Planar Ames-Cytotoxicity Bioassay Including Metabolic S9 Activation.Analytical chemistry · 2026Article
- Detection of Loss of Heterozygosity in Tk-Deficient Mutants from L5178Y TkMethods in molecular biology (Clifton, N.J.) · 2020Article
- Quantitative analysis of the relative mutagenicity of five chemical constituents of tobacco smoke in the mouse lymphoma assay.Mutagenesis · 2016Article
- Article
- Mechanistic evaluation of Ginkgo biloba leaf extract-induced genotoxicity in L5178Y cells.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Nitroxide TEMPO: a genotoxic and oxidative stress inducer in cultured cells.Toxicology in vitro : an international journal published in association with BIBRA · 2013Article
- Silver nanoparticle-induced mutations and oxidative stress in mouse lymphoma cells.Environmental and molecular mutagenesis · 2012Article
- Cytotoxicity and mutagenicity of retinol with ultraviolet A irradiation in mouse lymphoma cells.Toxicology in vitro : an international journal published in association with BIBRA · 2010Article
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6 authors at 2 institutions in 1 country.
Funding
Abstract
Retinyl palmitate (RP) is frequently used as an ingredient in cosmetics and other retail products. We previously reported that, under UVA light irradiation, RP is facilely decomposed into multiple products, including anhydroretinol (AR) and 5,6-epoxyretinyl palmitate (5,6-epoxy-RP). We also determined that combined treatment of mouse lymphoma cells with RP and UVA irradiation produced a photomutagenic effect. In this study, we evaluated the photomutagenicity of AR and 5,6-epoxy-RP, in L5178Y/Tk+/- mouse lymphoma cells. Treatment of cells with AR or 5,6-epoxy-RP alone at 10 and 25 microg/mL for 4 h did not show a positive mutagenic response. However, because these doses did not induce the required amount of cytotoxicity for mouse lymphoma assay, we are unable to determine whether or not these two compounds are mutagenic. Treatment of cells with 1-25 microg/mL AR or 5,6-epoxy-RP under UVA light (315-400 nm) for 30 min (1.38 mW/cm2) produced a synergistic photomutagenic effect. At 10 microg/mL (37.3 microM) AR with UVA exposure, the mutant frequency (MF) was about 3-fold higher than that for UVA exposure alone, whereas the MF for 25microg/mL (46.3microM) of 5,6-epoxy-RP + UVA was approximately 2-fold higher than that for UVA exposure alone. Compared with previous results for RP + UVA treatment, the potency of the induced phototoxicity and photomutagenicity was AR > RP > 5,6-epoxy-RP. To elucidate the underlying photomutagenic mechanism, we examined the loss of heterozygosity (LOH) at four microsatellite loci spanning the entire chromosome 11 for mutants induced by AR or 5,6-epoxy-RP. Most mutants lost the Tk+ allele, and more than 70% of the chromosome damage extended to 38 cM in chromosome length. AR + UVA induced about twice as many mutants that lost all four microsatellite markers from the chromosome 11 carrying the Tk+ allele as RP + UVA or 5,6-epoxy-RP + UVA. These results suggest that two of RP's photodecomposition products are photomutagenic in mouse lymphoma cells, causing events that affect a large segment of the chromosome.
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