Difference In 8-OHdG Levels Research Articles

Plasma 8-Hydroxydeoxyguanosine, 4-Hydroxynonenal and Selenium in Hepatitis B Virus-Infected Adults in Ibadan, Nigeria

Introduction: Hepatitis B Virus (HBV) infection is a significant global health challenge, particularly in Sub-Saharan Africa, including Nigeria. Reactive oxidative species (ROS) generated during HBV replication contribute to redox imbalance, leading to oxidative stress. However, data on the levels of oxidative stress markers in Nigerians infected with HBV is scarce. This study aimed to investigate plasma levels of oxidative stress markers [8-hydroxydeoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE)] and the trace element, selenium, in HBV-infected adults in Ibadan, Nigeria. Materials and Methods: In a case-control study, 40 HBV-infected patients served as cases, and 40 HBV-uninfected patients served as controls. Anthropometric data were collected, and plasma 8-OHdG and 4-HNE were determined using the ELISA method. Selenium was determined using atomic absorption spectrophotometry. Data were analysed using descriptive, t-test, and Pearson correlation statistics at p = 0.05. Results: The mean ages of HBV-infected and uninfected individuals were 35.3±1.5 and 36.0±1.5 years, respectively. The level of 4-HNE was not significantly different between HBV-infected (2.2±1.7 ng/ml) and uninfected (1.8±1.3 ng/ml). There was also no significant difference in 8-OHdG levels between HBV-infected (4.1±2.4 ng/ml) and uninfected (3.6±1.8 ng/ml). However, in HBV-infected patients, 8-OHdG levels showed a significant positive correlation with 4-HNE (r =0.320, p =0.044). Selenium levels were also significantly higher in HBV-infected (78.4±25.4 ug/dl) than uninfected (35.6±11.4 ug/dl). Conclusion: The levels of markers of lipid peroxidation and DNA oxidation were similar in HBV-infected and uninfected participants, but selenium, the key component of the potent antioxidant glutathione peroxidase was more than double in the infected group. It is plausible that the protective effect of Se may have spared the other markers of oxidative damage. Further studies are needed to elucidate these preliminary findings.

Simulated Microgravity Alters Gene Regulation Linked to Immunity and Cardiovascular Disease.

Microgravity exposure induces a cephalad fluid shift and an overall reduction in physical activity levels which can lead to cardiovascular deconditioning in the absence of countermeasures. Future spaceflight missions will expose crew to extended periods of microgravity among other stressors, the effects of which on cardiovascular health are not fully known. In this study, we determined cardiac responses to extended microgravity exposure using the rat hindlimb unloading (HU) model. We hypothesized that exposure to prolonged simulated microgravity and subsequent recovery would lead to increased oxidative damage and altered expression of genes involved in the oxidative response. To test this hypothesis, we examined hearts of male (three and nine months of age) and female (3 months of age) Long-Evans rats that underwent HU for various durations up to 90 days and reambulated up to 90 days post-HU. Results indicate sex-dependent changes in oxidative damage marker 8-hydroxydeoxyguanosine (8-OHdG) and antioxidant gene expression in left ventricular tissue. Three-month-old females displayed elevated 8-OHdG levels after 14 days of HU while age-matched males did not. In nine-month-old males, there were no differences in 8-OHdG levels between HU and normally loaded control males at any of the timepoints tested following HU. RNAseq analysis of left ventricular tissue from nine-month-old males after 14 days of HU revealed upregulation of pathways involved in pro-inflammatory signaling, immune cell activation and differential expression of genes associated with cardiovascular disease progression. Taken together, these findings provide a rationale for targeting antioxidant and immune pathways and that sex differences should be taken into account in the development of countermeasures to maintain cardiovascular health in space.

Level of 8-Hydroxy-2'Deoxyguanosine (8-OHdG) in children with acute lymphoblastic leukemia post-chemotherapy induction phase and post-chemotherapy maintenance phase

Introduction: Chemotherapy is an important curative therapy modality in ALL patients. 8-Hydroxy-2'-Deoxyguanosine (8-OHdG) has been studied as a biomarker of oxidative stress as a trigger for DNA damage, which is statistically significantly increased in ALL patients after chemotherapy compared to healthy children. This study aims to prove that 8-OHdG levels in children with ALL post-chemotherapy induction phases were higher than in the post-chemotherapy maintenance phase. Methods: This study used a cross-sectional design. The subjects were children aged 1-18 years, with ALL who received treatment at Prof Dr. I.G.N.G Ngoerah Hospital from September 2019-January 2021. The Mann-Whitney test assessed the 8-OHdG levels in children with ALL post-chemotherapy induction and post-chemotherapy maintenance phase. Logistic regression multivariate analysis was used to evaluate the factors that influence 8-OHdG levels in pediatric patients with ALL. The value of p<0,05 determined the level of significance. Results: A total of 27 subjects who underwent the post-chemotherapy induction phase and 19 subjects who underwent the post-chemotherapy maintenance phase were analyzed in this study. In the post-chemotherapy induction group, the median 8-OHdG level was 0.163 (0.104-1.864), and the median 8-OHdG level in the post-chemotherapy maintenance phase group was 0.158 (0.094-0.512). There was no significant difference in 8-OHdG levels between the two groups. Logistic regression multivariate analysis found that the post-chemotherapy induction phase was a prognostic factor at risk of increasing 8-OHdG levels (RO 16.55; 95% CI 1.118-245.277). Conclusion: This study concluded that 8-OHdG levels were higher in children post-chemotherapy induction phase than in children post-chemotherapy maintenance phase.

Assessment of 8-hydroxydeoxyguanosine levels in patients with preeclampsia: a prospective study

To determine the levels of 8-hydroxydeoxyguanosine (8-OHdG) in preeclampsia (PE) using (enzyme-linked immunosorbent assay (ELISA) method. Twenty-two pregnant women with severe PE, 18 pregnant women with mild PE, and 40 healthy pregnant women, all between 25 and 41 weeks of gestation, were enrolled in this prospective controlled study. 8-OHdG levels in maternal serum were measured using ELISA method. The authors observed no statistically significant difference in 8-OHdG levels between the mild-severe PE and control groups (p = 0.208). The present results do not support the concept that 8-OHdG has a role in the etiopathogenesis of PE.

8-Hydroxy-2-deoxyguanosine levels and heart failure: A systematic review and meta-analysis of the literature

Background and aimsThe generation of reactive oxygen species (ROS) plays an important role in the etiology of several pathological conditions. High levels of 8-hydroxy-2-deoxyguanosine (8-OHdG), a biomarker of oxidative damage of DNA, have been found in patients with heart failure (HF). We performed a meta-analysis of the literature to investigate the association between 8-OHdG levels and HF. Methods and resultsA systematic search was performed in the PubMed, Web of Science, Scopus, EMBASE databases and studies evaluating 8-OHdG levels in HF patients and controls were included. Differences between cases and controls were expressed as standard mean difference (SMD) or mean difference (MD) with pertinent 95% confidence intervals (95%CI). Impact of clinical and demographic features on effect size was assessed by meta-regression.Six studies (446 HF patients and 140 controls) were included in the analysis. We found that HF patients showed higher 8-OHdG levels than controls (SMD:0.89, 95%CI: 0.68, 1.10). The difference was confirmed both in studies in which 8-OHdG levels were assessed in urine (MD:6.28 ng/mg creatinine, 95%CI: 4.01, 8.56) and in blood samples (MD:0.36 ng/ml, 95%CI: 0.04, 0.69). Interestingly, 8-OHdG levels progressively increased for increasing New York Heart Association (NYHA) class. Meta-regression models showed that none of clinical and demographic variables impacted on the difference in 8-OHdG levels among HF patients and controls. Conclusions8-OHdG levels are higher in HF patients HF than in controls, with a progressive increase for increasing NYHA class. However, larger prospective studies are needed to test 8-OHdG as a biomarker of HF severity and progression.

8-Hydroxy-2-Deoxyguanosine Levels and Cardiovascular Disease: A Systematic Review and Meta-Analysis of the Literature.

Significance: 8-Hydroxy-2-deoxyguanosine (8-OHdG) is generated after the repair of ROS-mediated DNA damages and, thus, is one of the most widely recognized biomarkers of oxidative damage of DNA because guanosine is the most oxidized among the DNA nucleobases. In several pathological conditions, high urinary levels of oxidized DNA-derived metabolites have been reported (e.g., cancer, atherosclerosis, hypertension, and diabetes). Recent Advances: Even if published studies have shown that DNA damage is significantly associated with the development of atherosclerosis, the exact role of this damage in the onset and progression of this pathology is not fully understood, and the association of oxidative damage to DNA with cardiovascular disease (CVD) still needs to be more extensively investigated. We performed a meta-analysis of the literature to investigate the association among 8-OHdG levels and CVD. Critical Issues: Fourteen studies (810 CVD patients and 1106 controls) were included in the analysis. We found that CVD patients showed higher 8-OHdG levels than controls (SMD: 1.04, 95%CI: 0.61, 1.47, p < 0.001, I2 = 94%, p < 0.001). The difference was confirmed both in studies in which 8-OHdG levels were assessed in urine (MD: 4.43, 95%CI: 1.71, 7.15, p = 0.001) and in blood samples (MD: 1.42, 95%CI: 0.64, 2.21, p = 0.0004). Meta-regression models showed that age, hypertension, and male gender significantly impacted on the difference in 8-OHdG levels among CVD patients and controls. Future Directions: 8-OHdG levels are higher in patients with CVD than in controls. However, larger prospective studies are needed to test 8-OHdG as a predictor of CVD. Antioxid. Redox Signal. 24, 548–555.

Urinary 8-Hydroxy-2′-Deoxyguanosine: A Biomarker for Radiation-Induced Oxidative DNA Damage in Pediatric Cardiac Catheterization

To determine the utility of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) as a sensitive biomarker for radiation-induced cellular DNA damage in children undergoing cardiac catheterization. We enrolled pediatric patients with congenital heart diseases requiring cardiac catheterization in conjunction with healthy children and children under sedation as control. Demographic, clinical, laboratory and invasive hemodynamic data, urinary 8-OHdG levels, and radiation exposure measurements were collected prospectively. Nineteen patients, 10 healthy children and 9 children under sedation, were studied. In 19 patients who underwent cardiac catheterization, the median level of 8-OHdG in urine obtained at 24-48 hours after the procedure was significantly higher than at baseline (44.0 vs 17.3 ng/mg creatinine, P = .0001). Furthermore, the urinary 8-OHdG level after the procedure increased in 18 of the 19 study subjects. In contrast, there was no significant difference in 8-OHdG levels between the 2 spot urine samples obtained at arbitrary intervals of 24-48 hours in 10 healthy children (P = .7213), and at baseline and 24-48 hours following echocardiography in 9 children under sedation (P = .1097). Stepwise multiple regression analysis revealed that the cumulative air kerma during the cardiac catheterization was the variable which was strongly and significantly associated with the ratio of post- to precardiac catheterization urinary 8-OHdG levels among the evaluated variables (R(2) = 0.7179, F = 11.0256, P = .0007). Urinary 8-OHdG could be a useful biomarker for radiation-induced cellular DNA damage in children undergoing diagnostic cardiac catheterization.

Joint association of fruit, vegetable, and heterocyclic amine intake with DNA damage levels in a general population

ObjectiveTo assess joint effects of heterocyclic amine (HCA), fruit, and vegetable intake on DNA damage in a general population. MethodsA cross-sectional survey (ISA-Capital) was performed among adults and older adults in Brazil. We selected 73 participants with high HCA intake and 73 sex- and age-matched participants with non-HCA intake (n = 146) for the present study. Diet was assessed by a 24-h dietary recall and a structured questionnaire with cooking methods and levels of meat doneness. DNA damage was measured by 8-oxo-2′-deoxyguanosine (8-OHdG). The association between DNA damage and dietary intake was analyzed by linear regression models. ResultsFruit intake showed significantly inverse association with 8-OHdG (β, −0.787; P = 0.035), whereas HCA intake was significantly associated with increased DNA damage (β, 1.621; P = 0.036) after adjusting for covariates, including sex, age, body mass index, energy intake, smoking, physical activity, and C-reactive protein. Vegetable intake was not significantly associated with 8-OHdG. We also found a significant association between joint fruit and HCA intake and DNA damage, and the difference in 8-OHdG levels was significantly higher between participants with the lowest fruit intake and highest HCA intake and those with the highest fruit intake and non-HCA intake (P = 0.049). ConclusionsLower intake of fruits and higher intake of HCAs were associated with higher DNA damage levels and showed an additive effect pattern.

F14 8OHdG is not a biomarker for Huntington's disease; lessons for future biomarker studies

<h3>Background</h3> No candidate blood, CSF or urine biomarkers for HD have been clinically validated. 8-hydroxy-deoxy-guanosine (8OHdG) has been proposed as a candidate biomarker. Increased levels of 8OHdG have been reported in post-mortem brains^{1 2} and in serum,³ leucocytes⁴ and plasma⁵ of HD patients. All of the published studies on 8OHdG utilised a liquid chromatography electrochemical array (LCECA) assay. <h3>Aims</h3> To evaluate the potential of plasma 8-OHdG as a biomarker of HD state or progression and to develop a general set of procedures to test potential biomarkers. <h3>Methods</h3> We established a new liquid chromatography-mass spectrometry (LCMS) assay for 8OHdG and used it to measure 8OHdG levels in a cross-sectional plasma collection from the PREDICT-HD study. Next, longitudinal plasma samples taken 24 months apart from 160 TRACK-HD subjects, along with control plasma with added (“spiked”) 8OHdG, were sent blindly to two laboratories for measurement of 8OHdG using either the LCECA or the LCMS assay. <h3>Results</h3> We found no differences in 8OHdG levels between controls, premanifest HD and clinically diagnosed HD subjects from the PREDICT-HD study using the LCMS assay. A blinded head to head comparison showed the LCMS assay to be more accurate than the LCECA assay at measuring 8OHdG from spiked control plasma. Both assays were consistent in demonstrating no cross sectional differences in plasma 8OHdG between TRACK-HD controls, premanifest HD and early symptomatic HD subjects, and no longitudinal changes in any of the disease groups over 24 month. <h3>Conclusions</h3> Plasma concentration of 8-OHdG should not be considered a potential biomarker of disease state or disease progression in HD. To avoid the errors that have plagued such analyses, studies of all putative biomarkers should employ (1) blinded sample analyses; (2) verification of measurements by independent analytic methods; (3) standard curves; and (4) collection and storage of biological fluids under strict quality control. <h3>References</h3> 1. <b>Browne SE</b>, Bowling AC, MacGarvey U, <i>et al.</i> Oxidative damage and metabolic dysfunction in Huntington9s disease: selective vulnerability of the basal ganglia. <i>Ann Neurol</i> 1997;<b>41</b>:646–53. 2. <b>Polidori MC</b>, Mecocci P, Browne SE, <i>et al.</i> Oxidative damage to mitochondrial DNA in Huntington9s disease parietal cortex. <i>Neurosci Lett</i> 1999;<b>272</b>:53–6. 3. <b>Hersch SM</b>, Gevorkian S, Marder K, <i>et al.</i> Creatine in Huntington disease is safe, tolerable, bioavailable in brain and reduces serum 8OH29dG. <i>Neurology</i> 2006;<b>66</b>:250–2. 4. <b>Chen C</b>, Wu Y, Cheng M, <i>et al.</i> Increased oxidative damage and mitochondrial abnormalities in the peripheral blood of Huntington9s disease patients. <i>Biochem Biophys Res Commun</i> 2007;<b>359</b>:335–40. 5. <b>Long JD</b>, Matson WR, Juhl AR, <i>et al</i>; PREDICT-HD Investigators and Coordinators of the Huntington Study Group. 8OHdG as a marker for Huntington disease progression. <i>Neurobiol Dis</i> 2012;<b>46</b>:625–34.

The expression of 8-hydroxydeoxyguanosine in oesophageal tissues and tumours

Purpose The most common marker of oxidative DNA damage is 8-hydroxydeoxyguanosine (8-OHdG), which is linked with several malignancies. In the present study we investigated whether DNA damage linked to oxidative stress (as 8-OHdG) is present in Barrett's mucosa with or without associated adenocarcinoma or high-grade dysplasia and in normal controls' squamous mucosa. Experimental design We measured 8-OHdG in 51 patients (13 Barrett's metaplasia, six Barrett's oesophagus with high-grade dysplasia, 18 adenocarcinoma of the distal oesophagus/oesophagogastric junction and 14 normal controls). The amount of DNA damage was determined by high-performance liquid chromatography in oesophagus samples obtained either from endoscopy or as samples from surgery. The median 8-OHdG concentration was expressed as the ratio of 8-OHdG per 10 5 deoxyguanosine. Results Analysis revealed that 8-OHdG was present in both Barrett's metaplasia with and without dysplasia as well as in adenocarcinoma of the oesophagus/oesophagogastric junction. Although the study group was small the amount of 8-OHdG was significantly increased in the distal oesophagus both in Barrett's epithelium 1.26 (0.08–29.47) and in high-grade dysplasia 1.35 (1.04–1.65) as well as in adenocarcinoma of oesophagus/oesophagogastric junction 1.08 (0.59–1.94) compared to controls 0.06 (0–4.08) ( p = 0.002, p = 0.012, p = 0.001, respectively). Barrett's patients had no significant difference in 8-OHdG levels between their distal and proximal oesophageal samples. Conclusions Our results show the presence of oxidative DNA damage in the distal oesophagus of patients with Barrett's oesophagus and adenocarcinoma of the oesophagus/oesophagogastric junction. This may have a connection to carcinogenesis in Barrett's oesophagus.