Genotoxicity, recombinogenicity and cellular preneoplasic transformation induced by vitamin A supplementation
Autor: | Heloisa Helena Rodrigues de Andrades, Fábio Klamt, Rodrigo Juliani Siqueira Dalmolin, João Antonio Pêgas Henriques, Jenifer Saffi, Ana Ligia Lia de Paula Ramos, José Cláudio Fonseca Moreira, Ramatis Birnfeld de Oliveira, Rafael Roehrs, Felipe Dal-Pizzol |
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Rok vydání: | 2003 |
Předmět: |
Male
DNA Repair DNA damage Health Toxicology and Mutagenesis DNA Fragmentation Biology medicine.disease_cause Chinese hamster chemistry.chemical_compound Cricetulus Cricetinae Genetics medicine Animals Vitamin A Cells Cultured Recombination Genetic Mutagenicity Tests Retinol Sertoli cell biology.organism_classification Molecular biology Rats Comet assay medicine.anatomical_structure Cell Transformation Neoplastic Drosophila melanogaster chemistry Dietary Supplements DNA fragmentation Carcinogenesis Genotoxicity DNA Damage |
Zdroj: | Mutation research. 539(1-2) |
ISSN: | 0027-5107 |
Popis: | In spite of being one of the first vitamins to be discovered, the full range of biological activities of Vitamin A remains incomplete. A growing body of evidence has demonstrated an apparent enhancement of carcinogenesis, induced by dietary retinol. Since DNA damage is a well-recognized inducer of carcinogenesis, the aim of this study was to test the possible genotoxic effect of dietary retinol, using different types of bioassays. Retinol caused an increased recombinogenic activity in Drosophila melanogaster larvae as measured by the SMART test. In mammalian cell cultures, retinol supplementation-induced DNA double-strands breaks (DSB) and single-strands breaks (SSB), cell cycle progression and proliferative focus formation in terminal-differentiated rat Sertoli cells and increased DNA fragmentation in Chinese hamster lung fibroblasts (V79 cells), as measured by the comet assay. Altogether, our results suggest that retinol causes DNA damage and chromosomal rearrangements, which may disturbs key physiological processes and lead to cell cycle progression and preneoplasic transformation of terminal-differentiated mammalian cells. |
Databáze: | OpenAIRE |
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