Wavelength‐ and Tissue‐dependent Variations in the Mutagenicity of Cyclobutane Pyrimidine Dimers in Mouse Skin

2019 ◽  
Vol 96 (1) ◽  
pp. 94-104 ◽  
Author(s):  
Hironobu Ikehata ◽  
Toshio Mori ◽  
Yasuhiro Kamei ◽  
Thierry Douki ◽  
Jean Cadet ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers

scholarly journals Quantitative analysis of UV photolesions suggests that cyclobutane pyrimidine dimers produced in mouse skin by UVB are more mutagenic than those produced by UVC

2018 ◽  
Vol 17 (4) ◽  
pp. 404-413 ◽  
Author(s):  
Hironobu Ikehata ◽  
Toshio Mori ◽  
Thierry Douki ◽  
Jean Cadet ◽  
Masayuki Yamamoto
Keyword(s):  
Quantitative Analysis ◽  
Transgenic Mice ◽  
Mouse Skin ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Mutation Assay

The quantification of UV photolesions with a calibrated ELISA and the mutation assay with transgenic mice revealed that the molecular genotoxicity of CPDs depends on UVR components and skin tissues.

scholarly journals UVA1 Genotoxicity Is Mediated Not by Oxidative Damage but by Cyclobutane Pyrimidine Dimers in Normal Mouse Skin

2008 ◽  
Vol 128 (9) ◽  
pp. 2289-2296 ◽  
Author(s):  
Hironobu Ikehata ◽  
Kazuaki Kawai ◽  
Jun-ichiro Komura ◽  
Ko Sakatsume ◽  
Liangcheng Wang ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Normal Mouse ◽  
Mouse Skin ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers

scholarly journals Repurposing INCI-registered compounds as skin prebiotics for probiotic Staphylococcus epidermidis against UV-B

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Arun Balasubramaniam ◽  
Prakoso Adi ◽  
Do Thi Tra My ◽  
Sunita Keshari ◽  
Raman Sankar ◽  
...  
Keyword(s):  
Bacterial Species ◽  
Protective Action ◽  
Mouse Skin ◽  
Short Chain Fatty Acids ◽  
Skin Lesions ◽  
Ultraviolet B ◽  
Cyclobutane Pyrimidine Dimers ◽  
Pyrimidine Dimers ◽  
Cosmetic Ingredients ◽  
Genes Encoding

AbstractRepurposing existing compounds for new indications may facilitate the discovery of skin prebiotics which have not been well defined. Four compounds that have been registered by the International Nomenclature of Cosmetic Ingredients (INCI) were included to study their abilities to induce the fermentation of Staphylococcusepidermidis (S. epidermidis), a bacterial species abundant in the human skin. Liquid coco-caprylate/caprate (LCC), originally used as an emollient, effectively initiated the fermentation of S. epidermidis ATCC 12228, produced short-chain fatty acids (SCFAs), and provoked robust electricity. Application of LCC plus electrogenic S. epidermidis ATCC 12228 on mouse skin significantly reduced ultraviolet B (UV-B)-induced injuries which were evaluated by the formation of 4-hydroxynonenal (4-HNE), cyclobutane pyrimidine dimers (CPD), and skin lesions. A S. epidermidis S2 isolate with low expressions of genes encoding pyruvate dehydrogenase (pdh), and phosphate acetyltransferase (pta) was found to be poorly electrogenic. The protective action of electrogenic S. epidermidis against UV-B-induced skin injuries was considerably suppressed when mouse skin was applied with LCC in combination with a poorly electrogenic S. epidermidis S2 isolate. Exploring new indication of LCC for promoting S. epidermidis against UV-B provided an example of repurposing INCI-registered compounds as skin prebiotics.

scholarly journals A Role for Histone H2B During Repair of UV-Induced DNA Damage in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 160 (4) ◽  
pp. 1375-1387
Author(s):  
Emmanuelle M D Martini ◽  
Scott Keeney ◽  
Mary Ann Osley
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Chromatin Structure ◽  
Specific Effect ◽  
Cell Killing ◽  
Cyclobutane Pyrimidine Dimers ◽  
Histone H2b ◽  
Uv Sensitivity ◽  
Pyrimidine Dimers

Abstract To investigate the role of the nucleosome during repair of DNA damage in yeast, we screened for histone H2B mutants that were sensitive to UV irradiation. We have isolated a new mutant, htb1-3, that shows preferential sensitivity to UV-C. There is no detectable difference in bulk chromatin structure or in the number of UV-induced cis-syn cyclobutane pyrimidine dimers (CPD) between HTB1 and htb1-3 strains. These results suggest a specific effect of this histone H2B mutation in UV-induced DNA repair processes rather than a global effect on chromatin structure. We analyzed the UV sensitivity of double mutants that contained the htb1-3 mutation and mutations in genes from each of the three epistasis groups of RAD genes. The htb1-3 mutation enhanced UV-induced cell killing in rad1Δ and rad52Δ mutants but not in rad6Δ or rad18Δ mutants, which are defective in postreplicational DNA repair (PRR). When combined with other mutations that affect PRR, the histone mutation increased the UV sensitivity of strains with defects in either the error-prone (rev1Δ) or error-free (rad30Δ) branches of PRR, but did not enhance the UV sensitivity of a strain with a rad5Δ mutation. When combined with a ubc13Δ mutation, which is also epistatic with rad5Δ, the htb1-3 mutation enhanced UV-induced cell killing. These results suggest that histone H2B acts in a novel RAD5-dependent branch of PRR.

scholarly journals The effect of flanking bases on direct and triplet sensitized cyclobutane pyrimidine dimer formation in DNA depends on the dipyrimidine, wavelength and the photosensitizer

2021 ◽  
Author(s):  
Chen Lu ◽  
Natalia Eugenia Gutierrez-Bayona ◽  
John-Stephen Taylor
Keyword(s):  
Uv Light ◽  
Pyrimidine Dimer ◽  
Flanking Sequence ◽  
Quenching Mechanism ◽  
Cyclobutane Pyrimidine Dimers ◽  
Sequence Dependence ◽  
Pyrimidine Dimers ◽  
Skin Cancers ◽  
A Charge ◽  
C To T Mutations

Abstract Cyclobutane pyrimidine dimers (CPDs) are the major products of DNA produced by direct absorption of UV light, and result in C to T mutations linked to human skin cancers. Most recently a new pathway to CPDs in melanocytes has been discovered that has been proposed to arise from a chemisensitized pathway involving a triplet sensitizer that increases mutagenesis by increasing the percentage of C-containing CPDs. To investigate how triplet sensitization may differ from direct UV irradiation, CPD formation was quantified in a 129-mer DNA designed to contain all 64 possible NYYN sequences. CPD formation with UVB light varied about 2-fold between dipyrimidines and 12-fold with flanking sequence and was most frequent at YYYR and least frequent for GYYN sites in accord with a charge transfer quenching mechanism. In contrast, photosensitized CPD formation greatly favored TT over C-containing sites, more so for norfloxacin (NFX) than acetone, in accord with their differing triplet energies. While the sequence dependence for photosensitized TT CPD formation was similar to UVB light, there were significant differences, especially between NFX and acetone that could be largely explained by the ability of NFX to intercalate into DNA.

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