Abstract
Abstract Thyroidhormonesstimulateaerobicmetabolismwhichmayleadtooxidativestressaccompaniedbydamagetovari-ous cellular macromolecules, including DNA. Previous comet assay studies have shown that thyroid hormonescause DNA damage due to the creation of reactive oxygen species (ROS). However, cytogenetic studies have beenequivocal because although an increase in the sister-chromatid exchange frequency per cell has been reported in-creasedmicronucleifrequencyhasnot.Weusedcytogeneticexaminationofchromosomebreakageandaberrationsinwhole-bloodculturesofhumanperipheralbloodlymphocytestoinvestigatepossibleclastogeniceffectswhenlym-phocytes were exposed to 0.002 μMto50μM of L-thyroxine for 24 h and 48 h, these concentrations being chosenbecausetheyhadbeenusedinpreviousstudiesofsister-chromatidexchangeandmicronucleifrequency.Underourexperimental conditions thyroxine did not induced any statistically significant increase in chromosome breakage oraberrations. This lack of clastogenic effects is in contrast to the reported comet assay results obtained using purifiedlymphocytes, possibly because whole-blood cultures contain catalase and glutathione peroxidase capable of reduc-ing the effects of reactive oxygen species.
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