Divisão de Pesquisa

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https://dspace.inc.saude.gov.br/handle/123456789/18

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Navegando Divisão de Pesquisa por Autor "Arpini, Anna Paula"

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    DNA damage and repair in patients undergoing myocardial perfusion single‐photon emission computed tomography
    (Scientifc Reports, 2024) Lorenzo, Andrea de; Fernandes, Maria Clara dos Santos; Romeiro, Francisco; Arpini, Anna Paula; Dias, Glauber Monteiro
    As patient exposure to ionizing radiation from medical imaging and its risks are continuing issues, this study aimed to evaluate DNA damage and repair markers after myocardial perfusion single-photon emission computed tomography (MPS). Thirty-two patients undergoing Tc-99m sestamibi MP were studied. Peripheral blood was collected before radiotracer injection at rest and 60–90 min after injection. The comet assay (single-cell gel electrophoresis) was performed with peripheral blood cells to detect DNA strand breaks. Three descriptors were evaluated: the percentage of DNA in the comet tail, tail length, and tail moment (the product of DNA tail percentage and tail length). Quantitative PCR (qPCR) was performed to evaluate the expression of fve genes related to signaling pathways in response to DNA damage and repair (ATM, ATR, BRCA1, CDKN1A, and XPC). Mann–Whitney’s test was employed for statistical analysis; p< 0.05 was considered signifcant. Mean Tc-99m sestamibi dose was 15.1 mCi. After radiotracer injection, comparing post-exposure to pre-exposure samples o each of the 32 patients, no statistically signifcant diferences of the DNA percentage in the tail, tail length or tail moment were found. qPCR revealed increased expression of BRCA1 and XPC, without any signifcant diference regarding the other genes. No signifcant increase in DNA strand breaks was detected after a single radiotracer injection for MPS. There was activation of only two repair genes, which may indicate that, in the current patient sample, the efects of ionizing radiation on the DNA were not large enough to trigger intense repair responses, suggesting the absence of signifcant DNA damage.