Data/hora: 04/06/2024 05:15:11

Provedor de dados: | 74
País: | Brazil
Título: | Lack of clastogenic effects of L-thyroxine in whole-blood cultured human lymphocytes
Autores: | Djelic,Ninoslav; Djelic,Dijana; Spremo-Potparevic,Biljana; Zivkovic,Lada; Markovic,Biljana; Lozance,Olivera; Blagojevic,Milos.
Data: | 2007-01-01
Ano: | 2007
Palavras-chave: | Thyroxine; Human lymphocytes; Chromosome aberrations; Mitotic index; ROS.
Resumo: | Thyroid hormones stimulate aerobic metabolism which may lead to oxidative stress accompanied by damage to various cellular macromolecules, including DNA. Previous comet assay studies have shown that thyroid hormones cause DNA damage due to the creation of reactive oxygen species (ROS). However, cytogenetic studies have been equivocal because although an increase in the sister-chromatid exchange frequency per cell has been reported increased micronuclei frequency has not. We used cytogenetic examination of chromosome breakage and aberrations in whole-blood cultures of human peripheral blood lymphocytes to investigate possible clastogenic effects when lymphocytes were exposed to 0.002 µM to 50 µM of L-thyroxine for 24 h and 48 h, these concentrations being chosen because they had been used in previous studies of sister-chromatid exchange and micronuclei frequency. Under our experimental conditions thyroxine did not induced any statistically significant increase in chromosome breakage or aberrations. This lack of clastogenic effects is in contrast to the reported comet assay results obtained using purified lymphocytes, possibly because whole-blood cultures contain catalase and glutathione peroxidase capable of reducing the effects of reactive oxygen species.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572007000600019
Editor: | Sociedade Brasileira de Genética
Relação: | 10.1590/S1415-47572007000600019
Formato: | text/html
Fonte: | Genetics and Molecular Biology  v.30 n.4 2007
Fonte: | info:eu-repo/semantics/openAccess