8-hydroxy-2--deoxyguanosine has been researched along with Airway-Obstruction* in 2 studies
2 other study(ies) available for 8-hydroxy-2--deoxyguanosine and Airway-Obstruction
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Serum 8-hydroxy-2-deoxyguanosine as a marker of DNA oxidative damage in horses with recurrent airway obstruction.
It has been reported that equine recurrent airway obstruction (RAO) is a state of oxidative stress. Oxidant-antioxidant imbalance is known to increase the conversion of deoxyguanosine to 8-hydroxy-2-deoxyguanosine (8-OHdG) in DNA. 8-OHdG can easily be measured using ELISA tests in serum or urine samples. In this study, we analysed serum 8-OHdG levels in horses with recurrent airway obstruction and in healthy controls.. The study material consisted of seven healthy horses and seven horses with symptomatic RAO. All horses were exposed to moldy hay and straw for 48 h to induce clinical exacerbation of RAO. The serum 8-OHdG levels were determined using the ELISA Highly Sensitive 8-OHdG kit. The difference between the levels of 8-OHdG in healthy and RAO-affected horses was significant. The median level of 8-OHdG was 0.044 ng/ml in the healthy controls versus 0.498 ng/ml in RAO horses (P = 0.0021).. The results of the study strongly suggest that DNA damage coexists in the course of equine RAO. We therefore propose that future research should aim at the development of new drugs that target pro-inflammatory molecules, since DNA damage appears to be the result of chronic inflammation. Topics: 8-Hydroxy-2'-Deoxyguanosine; Airway Obstruction; Animals; Biomarkers; Deoxyguanosine; DNA; Enzyme-Linked Immunosorbent Assay; Horse Diseases; Horses; Inflammation; Oxidative Stress | 2016 |
DNA damage in children with obstructive adenotonsillar hypertrophy.
The objective of this prospective, controlled study was to evaluate oxidative DNA damage in children with obstructive adenotonsillar hypertrophy. This study included 30 patients with obstructive adenotonsillar hypertrophy (male/female ratio, 3:2; age range, 3-9 y) scheduled to undergo tonsillectomy and adenoidectomy and 25 control subjects of similar age and sex with no adenotonsillar disease or airway obstruction. Urine and blood samples were obtained from each child for 8-hydroxy 2-deoxyguanosine (8-OhdG) and malondialdehyde (MDA) concentrations. There were significant differences in leukocyte (3.28 [0.69/10] vs 0.70 [0.15/10] dG) and urine 8-OhdG (8.22 [2.27/10] vs 5.26 [1.3/10] dG) levels in patients with obstructive adenotonsillar hypertrophy and healthy subjects (P < 0.001 for both). Plasma (2.98 [1.31] vs 1.14 [0.64] μM) and urine (1.77 [0.84] vs 0.56 [0.32] μM) MDA levels were also different (P < 0.001 for both). There were positive correlations between 8-OhdG in leukocyte DNA and plasma MDA (r = 0.648, P < 0.001) and between levels of urine 8-OhdG excretion and urine MDA (r = 0.588, P < 0.001). The DNA damage in children with adenotonsillar hypertrophy should be kept in mind, but further studies must be done with larger patient groups. Topics: 8-Hydroxy-2'-Deoxyguanosine; Adenoidectomy; Adenoids; Airway Obstruction; Case-Control Studies; Child; Child, Preschool; Deoxyguanosine; DNA Damage; Female; Humans; Hypertrophy; Leukocytes; Male; Malondialdehyde; Oxidative Stress; Palatine Tonsil; Prospective Studies; Tonsillectomy | 2014 |