The goal of this investigation was to correlate the melanin content in human pigmentary cells with the generation of UVB-induced photoproducts and to examine the relationship between the melanin content and the removal of the photoproducts. Cultured melanocytes from light-skinned individuals synthesized less melanin and produced more cyclobutane pyrimidine dimers and 6-4 photoproducts upon UVB exposure than did melanocytes from black skin. Tyrosine-stimulated melanogenesis provided protection against DNA damage in both cell types. In another set of pigmented cell lines a ratio between eumelanin and pheomelanin was determined. The assessment of association between DNA damage induction and the quantity and quality of melanin revealed that eumelanin concentration correlated better with DNA protection than pheomelanin. Skin type-I and skin type-VI melanocytes, congenital nevus (CN)-derived cells and skin type-II melanocytes from a multiple-melanoma patient were grown in media with low or high L-tyrosine concentration. The cells were irradiated with 200 J/m2 UVB, and the levels of the photoproducts were determined immediately and after 6 and 24 h. Once again the induction of the photoproducts was mitigated by increased melanogenesis, and it was inversely correlated with the skin type. No significant differences were found for the removal of photoproducts in the cultures of skin types I and VI and CN cells. No indications of a delay in the removal of photoproducts in the melanocytes from the multiple-melanoma patient were found either.
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http://dx.doi.org/10.1562/0031-8655(2001)074<0424:mopaio>2.0.co;2 | DOI Listing |
Proc Natl Acad Sci U S A
October 2024
Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7260.
DNA repair processes modulate genotoxicity, mutagenesis, and adaption. Nucleotide excision repair removes bulky DNA damage, and in , basal excision repair, carried out by UvrA, B, C, and D, with DNA PolI and DNA ligase, occurs genome-wide. In transcription-coupled repair (TCR), the Mfd protein targets template strand (TS) lesions that block RNA polymerase for accelerated repair by the basal repair enzymes.
View Article and Find Full Text PDFJ Hazard Mater
December 2024
School of Environmental Science and Engineering, Huazhong University of Science and Technology, Wuhan 430074, PR China. Electronic address:
J Colloid Interface Sci
January 2025
Laboratory of Electrochemical Devices based on Solid Oxide Proton Electrolytes, Institute of High Temperature Electrochemistry (RAS), Yekaterinburg 620990, Russian Federation; Laboratory of Alternative Energy Conversion Systems, Department of Mechanical Engineering, School of Engineering, University of Thessaly, Pedion Areos 38334, Greece. Electronic address:
Designing efficient dual-functional catalysts for photocatalytic oxygen reduction to produce hydrogen peroxide (HO) and photodegradation of dye pollutants is challenging. In this work, we designed and fabricated an S-scheme heterojunction (g-CN/ZnO composite photocatalyst) via one-pot calcination of a mixture of ZIF-8 and melamine in the KCl/LiCl molten salt medium. The KCN/ZnO composite produced 4.
View Article and Find Full Text PDFBMC Plant Biol
July 2024
Department of Plant Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Gronostajowa 7, Kraków, 30-387, Poland.
Background: 6 - 4 photoproducts are the second most common UV-induced DNA lesions after cyclobutane pyrimidine dimers. In plants, they are mainly repaired by photolyases in a process called photoreactivation. While pyrimidine dimers can be deleterious, leading to mutagenesis or even cell death, 6 - 4 photoproducts can activate specific signaling pathways.
View Article and Find Full Text PDFNucleic Acids Res
August 2024
Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich 8057, Switzerland.
The histone methyltransferase ASH1L, first discovered for its role in transcription, has been shown to accelerate the removal of ultraviolet (UV) light-induced cyclobutane pyrimidine dimers (CPDs) by nucleotide excision repair. Previous reports demonstrated that CPD excision is most efficient at transcriptional regulatory elements, including enhancers, relative to other genomic sites. Therefore, we analyzed DNA damage maps in ASH1L-proficient and ASH1L-deficient cells to understand how ASH1L controls enhancer stability.
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