Mary Wilson
Well-known member
Version 2
posted 16 Aug, 2022
DOI: https://doi.org/10.21203/rs.3.rs-1696049/v2
Muhammet Yusuf Tepebaşı[SUP]1, [/SUP]İlter İlhan[SUP]2, [/SUP]Esra Nurlu Temal[SUP]2, [/SUP]Okan Sancer[SUP]2, [/SUP]Önder Öztürk[SUP]2[/SUP]
Abstract
COVID-19 disease, which spreads all over the world, is a disease characterized by widespread inflammation and affecting many organs, especially the lungs. The resulting inflammation triggers the formation of reactive oxygen radicals and may cause oxidative DNA damage. A total of 95 patients with positive RT-PCR test and hospitalization were divided into three groups according to the severity of pneumonia as mild, moderate and severe/critical. Inflammation markers (Neutrophil lymphocyte ratio, serum reactive protein, procalcitonin etc.), IL-10 and IF γ levels were detected by enzyme-linked immunosorbent assay method. In the evaluation of oxidative damage, thiol, disulfide and IMA levels were measured spectrophotometrically. In the evaluation of oxidative DNA damage, the tail DNA percent parameter obtained by the comet assay method was used. As a result, we found that total thiol, native thiol and disulfide levels decreased significantly due to the increase in inflammation markers and cytokine levels in the severe/critical group. At the same time, we determined that there was an increase in the tail DNA percent level, that is, DNA damage, due to the increased oxidative effect. As a result, we found that increased inflammation and reactive oxygen species due to the increase in pneumonia increased in those with severe and severe pneumonia, which in turn damaged DNA. We think that it would be useful to follow up the DNA damage in these patients in terms of neurodegenerative diseases and cancer development.
https://assets.researchsquare.com/f...-b7c2-4bd3-987b-06891455160f.pdf?c=1660666450
posted 16 Aug, 2022
DOI: https://doi.org/10.21203/rs.3.rs-1696049/v2
Muhammet Yusuf Tepebaşı[SUP]1, [/SUP]İlter İlhan[SUP]2, [/SUP]Esra Nurlu Temal[SUP]2, [/SUP]Okan Sancer[SUP]2, [/SUP]Önder Öztürk[SUP]2[/SUP]
Abstract
COVID-19 disease, which spreads all over the world, is a disease characterized by widespread inflammation and affecting many organs, especially the lungs. The resulting inflammation triggers the formation of reactive oxygen radicals and may cause oxidative DNA damage. A total of 95 patients with positive RT-PCR test and hospitalization were divided into three groups according to the severity of pneumonia as mild, moderate and severe/critical. Inflammation markers (Neutrophil lymphocyte ratio, serum reactive protein, procalcitonin etc.), IL-10 and IF γ levels were detected by enzyme-linked immunosorbent assay method. In the evaluation of oxidative damage, thiol, disulfide and IMA levels were measured spectrophotometrically. In the evaluation of oxidative DNA damage, the tail DNA percent parameter obtained by the comet assay method was used. As a result, we found that total thiol, native thiol and disulfide levels decreased significantly due to the increase in inflammation markers and cytokine levels in the severe/critical group. At the same time, we determined that there was an increase in the tail DNA percent level, that is, DNA damage, due to the increased oxidative effect. As a result, we found that increased inflammation and reactive oxygen species due to the increase in pneumonia increased in those with severe and severe pneumonia, which in turn damaged DNA. We think that it would be useful to follow up the DNA damage in these patients in terms of neurodegenerative diseases and cancer development.
https://assets.researchsquare.com/f...-b7c2-4bd3-987b-06891455160f.pdf?c=1660666450
