We have addressed the question whether the level of UV-B induced DNA damage can be accurately assessed by the measurement of the rate of unscheduled DNA synthesis (UDS). Cultured human fibroblasts were irradiated with UV radiation at 290, 313 or 365 nm. The LD50 was 85 J/m2 at 290 nm, 4500 J/m2 at 313 nm, and 70 kJ/m2 at 365 nm. The analysis of UDS measurements indicate complete arrest of repair processes within 24 h after irradiation, irrespective of the dose (in the range 10-60 J/m2 at 290 nm, and 250-1000 J/m2 at 313 nm). Irradiation at 365 nm failed to yield detectable evidence of UDS. Incubation of irradiated cells with an antiserum directed against both 6-4 type and cyclobutane-type pyrimidine dimers shows a clear parallelism between the disappearance of the antibody-binding determinants and the variation of the rate of UDS vs time after the end of the irradiation. Thus it is concluded that in UV-B irradiated normal cultured human fibroblasts, the lack of UDS reflects the absence of immunodetectable pyrimidine dimers.
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Biomedicines
December 2024
Department of Nuclear Medicine, University Hospital Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany.
Energy delivered at different wavelengths causes different types of damage to DNA. PC-3, FaDu, 4T1 and B16-F10 cells were irradiated with different wavelengths of ultraviolet light (UVA/UVC) and ionizing radiation (X-ray). Furthermore, different photosensitizers (ortho-iodo-Hoechst33258/psoralen/trioxsalen) were tested for their amplifying effect.
View Article and Find Full Text PDFNutrients
December 2024
Department of Dermatology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Background/objective: Ultraviolet (UV) B radiation leads to DNA damage by generating cyclobutane pyrimidine dimers (CPDs). UVB-induced CPDs can also result in immune suppression, which is a major risk factor for non-melanoma skin cancer (NMSC). UVB-induced CPDs are repaired by nucleotide repair mechanisms (NER) mediated by xeroderma pigmentosum complementation group A (XPA).
View Article and Find Full Text PDFBiomolecules
November 2024
Laboratory of Molecular and Cell Biology, Istituto Dermopatico Dell'Immacolata (IDI-IRCCS), 00167 Rome, Italy.
UVB radiation induces DNA damage generating several thymine photo-adducts (TDPs), which can lead to mutations and cellular transformation. The DNA repair pathways preserve genomic stability by recognizing and removing photodamage. These DNA repair side products may affect cellular processes.
View Article and Find Full Text PDFCyclobutane pyrimidine dimers (CPDs) are formed in DNA following exposure to ultraviolet (UV) light and are mutagenic unless repaired by nucleotide excision repair (NER). It is known that CPD repair rates vary in different genome regions due to transcription-coupled NER and differences in chromatin accessibility; however, the impact of regional chromatin organization on CPD formation remains unclear. Furthermore, nucleosomes are known to modulate UV damage and repair activity, but how these damage and repair patterns are affected by the overarching chromatin domains in which these nucleosomes are located is not understood.
View Article and Find Full Text PDFFree Radic Biol Med
February 2025
Univ. Bordeaux, Inserm, BRIC, UMR 1312, F-33076, Bordeaux, France; Aquiderm, University of Bordeaux, Bordeaux, France. Electronic address:
Solar ultraviolet B (UVB) radiation-induced DNA damage is a well-known initiator of skin carcinomas. The UVB-induced DNA damage response (DDR) involves series of signaling cascades that are activated to maintain cell integrity. Among the different biological processes, little is known about the role of energy metabolism in the DDR.
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