Oxidative Deoxyribonucleic Acid Research Articles

Oxidative DNA Damage and Deranged Lipid Profile in Patients with Pulmonary Tuberculosis: A Cross-sectional Study

Introduction: Tuberculosis (TB) is one of the major health problems and a leading cause of death from infectious diseases. Oxidative damage in tuberculosis results from biochemical interactions between Reactive Oxygen Species (ROS) and target biomolecules. Increased oxidative stress leads to elevated Oxidative Deoxyribonucleic Acid (DNA) damage in Pulmonary Tuberculosis (PTB) patients. It is important to study serum lipids and oxidative DNA damage as they affect the overall immune system of individuals. Aim: To investigate deranged lipid profiles and oxidative DNA damage in PTB. Materials and Methods: A single-centered, cross-sectional study was conducted at Grant Government Medical College, Mumbai from October 2016 to November 2017. A total of 50 PTB patients in the age group of 20-60 years and 50 healthy subjects were included in the study. Oxidative DNA damage was assessed using 8-hydroxy-2-deoxyguanosine (8-OHdG) as a biomarker with a highly sensitive Enzyme-linked Immunosorbent Assay (ELISA) kit, and lipid profiles were estimated. An Unpaired t-test was used to analyse the significance of the study parameters in the cases and control groups. Results: The study involved 100 participants, predominantly males (63%), with most falling in the age group of 18-45 years (77%). The present study revealed significantly elevated levels (p-value <0.05) of 8-OHdG in patients; however, significantly reduced levels (p-value <0.05) of total cholesterol, Triglycerides (TG), High-density Lipoprotein cholesterol (HDL), Very Low- density Lipoprotein cholesterol (VLDL), and Low-density Lipoprotein cholesterol (LDL) were observed in cases compared to controls. Conclusion: The present study observed an increase in the level of 8-hydroxy-2-deoxyguanosine (8-OHdG), indicating greater oxidative DNA damage in tuberculosis patients due to oxidative stress, leading to lipid profile derangement.

Stromal inflammation, fibrosis and cancer: An old intuition with promising potential.

It is now well established that the biology of cancer is influenced by not only malignant cells but also other components of the tumour microenvironment. Chronic inflammation and fibrosis have long been postulated to be involved in carcinogenesis. Chronic inflammation can promote tumorigenesis via growth factor/cytokine-mediated cellular proliferation, apoptotic resistance, immunosuppression; and free-radical-induced oxidative deoxyribonucleic acid damage. Fibrosis could cause a perturbation in the dynamics of the tumour microenvironment, potentially damaging the genome surveillance machinery of normal epithelial cells. In this review, we will provide an in-depth discussion of various diseases characterised by inflammation and fibrosis that have been associated with an increased risk of malignancy. In particular, we will present a comprehensive overview of the impact of alterations in stromal composition on tumorigenesis, induced as a consequence of inflammation and/or fibrosis. Strategies including the application of various therapeutic agents with stromal manipulation potential and targeted cancer screening for certain inflammatory diseases which can reduce the risk of cancer will also be discussed.

Secondary Degeneration of Oligodendrocyte Precursor Cells Occurs as Early as 24 h after Optic Nerve Injury in Rats.

Optic nerve injury causes secondary degeneration, a sequela that spreads damage from the primary injury to adjacent tissue, through mechanisms such as oxidative stress, apoptosis, and blood-brain barrier (BBB) dysfunction. Oligodendrocyte precursor cells (OPCs), a key component of the BBB and oligodendrogenesis, are vulnerable to oxidative deoxyribonucleic acid (DNA) damage by 3 days post-injury. However, it is unclear whether oxidative damage in OPCs occurs earlier at 1 day post-injury, or whether a critical 'window-of-opportunity' exists for therapeutic intervention. Here, a partial optic nerve transection rat model of secondary degeneration was used with immunohistochemistry to assess BBB dysfunction, oxidative stress, and proliferation in OPCs vulnerable to secondary degeneration. At 1 day post-injury, BBB breach and oxidative DNA damage were observed, alongside increased density of DNA-damaged proliferating cells. DNA-damaged cells underwent apoptosis (cleaved caspase3+), and apoptosis was associated with BBB breach. OPCs experienced DNA damage and apoptosis and were the major proliferating cell type with DNA damage. However, the majority of caspase3+ cells were not OPCs. These results provide novel insights into acute secondary degeneration mechanisms in the optic nerve, highlighting the need to consider early oxidative damage to OPCs in therapeutic efforts to limit degeneration following optic nerve injury.

Oxidative DNA Damage in Relation to the Severity of COVID-19 Infection in Duhok City, Kurdistan Region- Iraq

Coronavirus disease 2019 (COVID-19) has rapidly spread across the globe since its outbreak in Wuhan, China, in 2019. Clinical evidence suggests higher oxidative stress in COVID-19 patients, and this worsening redox status which may contribute to disease progression. The present study aimed to investigate the oxidative Deoxyribonucleic acid damage in patients with mild and severe COVID-19 infection and to evaluate its relationship to the disease progression and severity. A case-control study was conducted from September 2021 to January 2022 in Duhok city, Kurdistan Region-Iraq. 180 individuals have participated. Among 88 COVID-19 cases, 92 healthy volunteers as the control group, with ages ranging (18-45) years. Patients were divided into two groups according to the severity of infection (mild cases, severe cases). Serum level of 8-OHdG and malondialdehyde (MDA) were assessed as oxidative stress biomarkers. Serum levels of 8-OHdG were considerably higher in patients with COVID-19 infection in comparison to the control group, (p<0.01). The further statistical analysis has revealed a significantly higher 8-OHdG in blood in female cases with severe COVID-19 infection compared cases with a mild infection, (p<0.01). Serum MDA levels in severe cases were higher, statistically significant when compared with the control group (p=0.007). Severe cases had higher level of MDA than in mild case, in male cases (p<0.05) in female cases (p<0.0001). The current data suggest that patients who were infected severely with COVID-19 are under huge oxidative stress attack. Analysis of data shows that severe cases of COVID-19 infection had significantly greater level of serum 8-OHdG than in healthy control subjects.

Evaluation of Oxidative DNA Damage among Type 2 Diabetes Mellitus Patients and Healthy Individuals in Duhok, Iraq: A Case-control Study

Introduction: The association between oxidative Deoxy Ribonucleic Acid (DNA) damage and diabetes is well established. Increased glucose levels can stimulate free radical production. However, data regarding DNA damage in type 2 Diabetes Mellitus (DM) patients and healthy individuals are controversial and scarce in Iraq. Aim: To assess the DNA damage among patients with type 2 Diabetes Mellitus (DM) and healthy individuals and to analyse its relationship with oxidative stress biomarkers. Materials and Methods: This case-control study was conducted at the Duhok Diabetes Center, Duhok, Kurdistan Region, Iraq, from September 2016 to March 2018. In this study, biomarkers of both oxidative stress and DNA damage including Total Antioxidant Capacity (TAC), Malondialdehyde (MDA) and serum 8-Hydroxy-2-deoxiguanosine (8-OHdG) were measured in 297 patients with type 2 diabetes and 188 healthy individuals. Selection of cases and healthy individuals was done using random sampling technique. Statistical analysis was done using Statistical Package for Social Sciences (SPSS) version 18.0 and a p-value <0.05 was set as a cut off value of statistical significance. Results: The mean age, sex and Body Mass Index (BMI) were similar between patients and healthy individuals. Significantly higher 8-OHdG and MDA levels (p<0.001 and p<0.010, respectively) together with lower TAC levels (p=0.010) were found in diabetics compared to healthy individuals. In diabetic patients, a positive correlation of 8-OHdG was observed with MDA (r=0.220), and a negative correlation was observed with TAC (r= -0.47). Based on the estimated cut-off point of DNA damage (8-OHdG of 4.0 ng/mL), 84.51% of patients had high levels of DNA damage compared with healthy individuals (28.7%). Conclusion: Oxidative DNA damage increased in diabetic patients, and was associated with lower antioxidant capacity. Antioxidant supplementation may be an effective public health intervention to reduce DNA damage and oxidative stress.

Nutraceutical Effects of Justicia carnea Leaf Powder Supplementations on Performance, Blood Indices, Heat Shock Protein 70, Oxidative Deoxyribonucleic Acid Damage Biomarkers and Intestinal Microbes of Broiler Chickens, Under Tropical Condition.

The main reason preventing broiler chickens from reaching their genetic potential and hurting their performance in the tropics is heat stress. This study aimed to ascertain how Justicia carnea leaf powder (JLP) supplementation affects broiler chickens' performance, blood indices, antioxidant status, and gut microflora in tropical environments. A completely randomized method was used to assign 240 Cobb 500 broiler chicks to the experimental diets (6 replicates per diet, 10 birds per replication). Diet 1 included no supplement (negative control), diet 2 included 200 mg/kg vitamin C (positive control), diet 3 included 2,500 mg/kg JLP, and diet 4 included 5,000 mg/kg JLP. On day 42, the body weight gain (BWG) of the birds fed on diet 4 was significantly higher than those on diet 1. The packed cell volume, red blood cell count, and hemoglobin concentration of the birds fed on diets 3 and 4 were significantly higher than those of the control (P<0.05). The serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and cholesterol were lower in birds fed on diets 3 and 4, compared to those on diet 1 (P<0.05). The serum heat shock protein 70 (HSP 70) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were lower in birds fed on diets 3 and 4, compared to those on diet 1 (P<0.05). The lactic acid-producing bacteria (LAB) population was higher in birds fed on diets 3 and 4, compared to those on diet 1(P<0.05). However, the Coliform bacteria population was reduced in birds fed on diets 3 and 4, compared to those on diet 1. The 2,500 and 5,000 mg/kg JLP dietary supplementations enhanced BWG, improved erythrogram indices, and reduced blood AST, ALT, cholesterol, HSP 70, 8-OHdG, and caeca Coliform population but increased the caeca LAB population.

Caffeic acid protects against DNA damage, oxidative and inflammatory mediated toxicities, and upregulated caspases activation in the hepatorenal system of rats treated with aflatoxin B1

Aflatoxicosis can induce largescale toxicities in predisposed populations. Food fortification with adequate antioxidant sources may reduce the toxic burden from aflatoxicosis. We examined the individual and combined effect of Caffeic acid (CA) on the aflatoxin B1 (AFB1)-induced hepatic and renal injury in male rats. Five experimental rat cohort (n = 6) consisting of the control (2 mL/kg corn oil), AFB1 alone (50 μg/kg), CA alone (40 mg/kg), AFB1+CA1 (50 μg/kg + 20 mg/kg) and AFB1+CA2 (50 μg/kg + 40 mg/kg) were so treated for 28 consecutive days. Upon sacrifices, diagnostic markers of hepatorenal functions, oxidative stress, inflammation, oxidative deoxyribonucleic acid -DNA-damage and apoptosis were analysed. Our results showed that CA reduced AFB1-induced toxicities in rats' liver and kidneys by significantly increasing (p < 0.05) endogenous antioxidant and the anti-inflammatory IL-10 level. Caffeic acid simultaneously reduced hepatic and renal dysfunction biomarkers in the serum, oxidative stress, and lipid peroxidation levels. Besides, CA diminished reactive oxygen and nitrogen species, inflammatory nitric oxide levels, interleukin-1 β and the activities of xanthine oxidase and myeloperoxidase. Additionally, CA reduced DNA damage and caspase-mediated apoptotic responses and preserved the cytoarchitecture of rats' liver and kidneys treated with AFB1. These data suggest that CA can be used as a food additive to mitigate AFB1-induced toxicity in the examined organs.

Protective Effects of Polyvinylpyrrolidone-Wrapped Fullerene Against Nitric Oxide/Peroxynitrite-Induced Cellular Injury in Human Skin Keratinocytes.

Excess ultraviolet (UV) exposure accelerates skin inflammation, melanogenesis, wrinkle formation, photoaging, and carcinogenesis through oxidative stress and deoxyribonucleic acid damage. These deleterious effects to skin are closely associated with UV-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) produced via nitric oxide (NO·) generation. RNS are known to be responsible for various skin disorders, such as erythema, melanin production, reduced barrier function, and psoriasis. These skin disorders are major cosmetic problems; RNS control, in addition to ROS control, is important for maintaining healthy skin. In the present study, we investigated the cytoprotective effects of polyvinylpyrrolidone-entrapped fullerene (C60/PVP), a water-soluble ROS scavenger, against nitric oxide (NO·) and peroxynitrite (ONOO-)-induced human keratinocyte injuries. Protective effects of C60/PVP on NO·/ONOO--induced cellular damage and intracellular ONOO- generation were evaluated using a NO· donor S-nitroso-N-acetylpenicillamine (SNAP) in human skin epidermal HaCaT keratinocytes. Furthermore, the suppressive effect of C60/PVP on UVB-induced generation of intracellular ONOO- levels was also investigated. C60/PVP exerted suppressive effects on intracellular increases in NO·-induced ONOO- generation and subsequent cellular damage. Additionally, C60/PVP significantly decreased the UVB-induced generation of intracellular ONOO- levels. These findings suggest that C60/PVP could be useful as a cosmetics ingredient for prevention of skin injuries and/or dysfunction from NO·/ONOO--induced effects in human skin keratinocytes.

8-Hydroxy-2-Deoxyguanosine as Oxidative DNA Damage Biomarker of Medical Ionizing Radiation: A Scoping Review.

Background: Recent studies reported the significant expansion using 8-Hydroxy-2-Deoxyguanosine (8-OHdG) as a biomarker of oxidative Deoxyribonucleic Acid (DNA) damage among human populations exposed to medical ionizing radiation, but a generalized overview about this topic has not been conducted yet. Objective: This scoping review of published literature examined recent trends in utilizing 8-OHdG biomarker to measure oxidative DNA damage induced by medical ionizing radiation and possible factors that may influence the 8-OHdG level.Material and Methods: Literature search was conducted in PubMed, Scopus and ProQuest databases for publications from 1984 to 2/12/2020. Included articles were: cohort studies, case-control studies, and cross–sectional studies, randomized and nonrandomized controlled trials. Excluded articles were: editorials, letters, personal opinions, newspaper articles, study plans, protocols, qualitative studies, case reports and series, in-vivo and vitro studies, animal research studies, reviews and meta-analyses. Results: According to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, we screened 141 articles, and 10 eligible studies met our inclusion criteria. All studies measured 8-OHdG as an oxidative DNA damage biomarker. The study results were contradictory concerning the relationship between the radiation dose and 8-OhdG level. 8-OHdG was mostly measured by enzyme-linked immunosorbent assay (ELISA) using urine samples. Sample size varied between (n=25-230) and included patients who underwent medical radiation procedures or workers exposed to ionizing radiation during their jobs. Conclusion: This scoping review findings showed 8-OHdG can be used as a promising biomarker to detect oxidative damage, resulting from medical ionizing radiation exposure despite external factors that may influence 8-OHdG levels.

Quercetin and its ester derivatives inhibit oxidation of food, LDL and DNA

Quercetin was esterified with fatty acids (FA) in order to expand its application in a wide range of food and biological systems. The antioxidant potential of the esters were examined using hydroxyl radical scavenging activity, antioxidation in oil-in-water emulsion and bulk oil, inhibition of low-density lipoprotein (LDL) oxidation and deoxyribonucleic acid (DNA) scission. Except for oil-in-water emulsion system, quercetin derivatives demonstrated similar and/or better antioxidant activity than quercetin itself in bulk oil (quercetin with C18:1 and C22:6), hydroxyl radical scavenging assay (quercetin with C3:0-C8:0), DNA scission (quercetin with C3:0-C8:0), and LDL oxidation (quercetin with C14:0-C22:6, except C18:0). These results suggest that esterification did not compromise the antioxidant activity of the parent compound and quercetin derivatives might be useful as possible antioxidants in food and biological systems.

Oxidative DNA damage and subclinical hypothyroidism in children with obesity

BackgroundObesity-related oxidation stress plays a key role in obesity complications; however, its relation to thyroid status is an area for further research. The study aimed to assess thyroid function in obese children and its relation to oxidative deoxyribonucleic acid (DNA) damage.ResultsFifty obese and 40 normal weight children were included. Anthropometric measurement, lipid profile, thyroid function, anti-thyroglobulin antibody, thyroid peroxidase antibody, and 8-hydroxydeoxyguanosine serum level as marker of oxidative DNA damage were measured. Thirty-six percent of children with obesity have subclinical hypothyroidism. Central obesity but not oxidative DNA damage and lipid profile was significantly associated with subclinical hypothyroidism. Waist circumference > 97th centile increases the risk for subclinical hypothyroidism (odd ratio 10.82; confidence interval 95% 2.75–42.409; p-value<0.001).ConclusionCentral obesity represents a risk factor for subclinical hypothyroidism in obese children. Oxidation DNA damage did not show significant association with subclinical hypothyroidism.

Preventive effect of Euphorbia royleana Boiss on diabetes induced by streptozotocin via modulating oxidative stress and deoxyribonucleic acid damage

Oxidative stress is associated with streptozotocin induced diabetes. The present study was conducted to investigate the anti-oxidant, anti-diabetic and genotoxic effects of Euphorbia royleana Boiss. stem’s crude extract in rats. Better inhibitory concentration (IC50) of methanolic extract in alpha amylase and antioxidant assays along with improvement in hyperglycemia can be linked with the presence of phenolic acids and flavonoids determined quantitatively by HPLC. The declining superoxide dismutase, catalase activities, and hydrogen peroxide concentrations were restored at the dose of 500 mg/kg. The methanolic extract turned out to be Class I genotoxic at 100 µg/mL. Moreover, improvement in histopathological changes of pancreas, liver and kidney were also observed.

Apocynin protects retina cells from ultraviolet radiation damage via inducing sirtuin 1

Direct exposure to Ultraviolet (UV) radiation causes progressive damages in retinal cells, which is one of the hypothetical mechanisms underlying age-related retinopathy or macular degeneration. The protective effects of Apocynin against UV damages were firstly tested in retinal pigment epithelium cells (RPEs) and retinal ganglion cells (RGCs). Subsequently the beneficial effect of Apocynin on mouse retinas against light damage were examined. Next, microarray profiling was used to identify the genes regulated by Apocynin in both RPEs and RGCs. A candidate gene was isolated for functional characterisation by knock-down study. Apocynin was shown to inhibit cell death, reduce oxidative stress and deoxyribonucleic acid damages in both RPEs and RGCs challenged with UV. Intravitreal application of Apocynin also improved retinal dysfunction caused by light damage. Sirtuin 1 (SIRT1) was identified as induced by Apocynin by microarray study. The induction was confirmed by realtime-PCR and western blotting. Knocking down SIRT1 antagonised the protective effect of Apocynin against UV damages in both RPEs and RGCs. Apocynin is a novel agent that shows both in vitro and in vivo efficacies against UV radiation induced retina damages. SIRT1 pathway is implicated in UV radiation protection of Apocynin in retinal cells.

Impact of DNA Oxidation on Toxicology: From Quantification to Genomics.

Understanding the toxicological implications of deoxyribonucleic acid (DNA) oxidation arising from cellular oxidative stress depends on identifying DNA oxidation products, their location in the genome, and their interaction with repair, replication, and gene expression.

Diabetes and obesity during pregnancy are associated with oxidative stress genotoxicity in newborns.

Objective To compare the level of oxidative deoxyribonucleic acid (DNA) damage (genotoxicity) between the offspring of mothers with and without diabetes diagnosed during pregnancy and its association with maternal body mass index (BMI). Methods We measured 8-hydroxy-deoxyguanosine (8-OH-dG), a marker of DNA oxidative damage, in venous umbilical cord plasma from newborns of mothers with (n=34) and without (n=56) diabetes diagnoses obtained during pregnancy. Two markers of oxidative stress - namely, nitric oxide degradation products (NOx) and total glutathione (GSH) - were quantified in both mothers and newborns. The effects of BMI, glycated hemoglobin (HbA1c), age and delivery mode were also analyzed. Results Newborns of mothers with diabetes during pregnancy exhibited higher levels of 8-OH-dG than those of mothers without diabetes (P<0.001). The other markers of oxidative stress were also higher in both mothers with diabetes and their newborns, with the exception of NOx in the mothers. The association of diabetes with 8-OH-dG was independent of other analyzed factors. Conclusion The offspring of mothers with diabetes during pregnancy are born with increased genotoxicity than the offspring of mothers without diabetes. BMI and HbA1c display an independent association with 8-OH-dG, particularly in the offspring of mothers not diagnosed with diabetes.

Western diet induces endogen oxidative deoxyribonucleic acid damage and infl ammation in Wistar rats

ABSTRACT Objective Nutritional diseases such as metabolic syndrome, cardiovascular disorder, chronic inflammation or even cancer are observed in people who sustain their lifestyle by Western diet due to high calorie intake. The origin of these diseases are the degraded deoxyribonucleic acid structure. In this study, we investigated whether Western diet produced endogenous oxidative deoxyribonucleic acid damage, apoptosis or inflammation. Methods Twenty-eight male Wistar rats, aged 10-12 weeks, were divided into four groups. The rats in control group received the standard diet and the remaining rats were given one of the following three diets for four weeks: a high-fat diet containing 35% fat, a high-sucrose diet containing 69% sucrose and Western diet comprising both two types of diets. After treatment the serum 8-hydroxy-2-deoxyguanosine, poly (adenosine diphosphate ribose) polymerase-1, chitinase-3-like protein 1, soluble urokinase-type plasminogen activator receptor, Fas ligand and cytochrome c levels were measured. Results It was observed no changes in the serum soluble urokinase-type plasminogen activator receptor, Fas ligand and cytochrome c levels whereas a statistically significant increase in the serum 8-hydroxy-2-deoxyguanosine, poly (adenosine diphosphate ribose) polymerase-1 and chitinase-3-like protein 1 levels were found only in rats that were given Western diet. Conclusion The findings show that Western diet produced endogenous oxidative deoxyribonucleic acid damage, which then increased serum poly (adenosine diphosphate ribose) polymerase-1 levels, eventually leading to inflammation.

Modulation of Phospho Tensin Homolog (PTEN) in Cancer Cells and Lipid Peroxides in Peripheral Blood Mononuclear Cells (PBMCs) Following Exposure to Flavonoids

Plant flavonoids have been shown to offer more protective health benefits against oxidative deoxyribonucleic acid (DNA) damages caused by γ‐ray radiation, UV irradiation, chemicals, and endogenous oxidative stress. The above compounds have been shown to be capable of modulating the activity of enzymes, and affect the behavior of many cell systems. While these may account for the anti‐mutagenic activities of flavonoids in experimental systems, relatively little is known about the mechanisms of the modulation of PTEN activity in cancer cells and the levels of lipid peroxides in peripheral blood mononuclear cells (PMBCs). The objectives of this study was to investigate the effects of three flavonoids: quercetin, kaempferol and genistein on the expression levels of both phospho‐ and total‐PTEN in breast cancer (BT‐549), lung cancer (A‐549) and human preadipocytes (3T3‐L1 which was used as controls). Furthermore, the effects of the flavonoids on lipid peroxides in PMBCs were investigated. Cells were seeded and were exposed to each of the flavonoid at concentrations of 0, 5, 10, 15, 20 and 25 μM and the phosphorylation of PTEN at Ser380, total PTEN levels, and lipid peroxides (i.e., malonaldehyde (MDA before and after the oxidative stress)) levels were measured. The results indicate the flavonoids increased both phospho‐PTEN‐ and total‐PTEN levels increased in a dose‐dependent manner. The effect of quercetin was more pronounced followed by genistein and kaempferol. Exposure of PMBCs cells to the various flavonoids at the different concentrations lowered the MDA levels compared to their respective controls. Levels of MDA in quercetin treated samples were lower compared to kaempferol and genistein. The findings suggest that the flavonoids play an important role in controlling oxidative stress in cells.Support or Funding InformationNational Institutes of Health: 2T34GM007663This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Nerium oleander Distillate Can Reduce Oxidative Deoxyribonucleic Acid Damage in Rats Fed with High Cholesterol Diet

Nerium oleander Distillate Can Reduce Oxidative Deoxyribonucleic Acid Damage in Rats Fed with High Cholesterol Diet

High serum levels of 8-OHdG are an independent predictor of post-stroke depression in Chinese stroke survivors.

PurposeAlthough previous studies have investigated oxidative stress biomarkers in association with depression in non-stroke subjects, the association between oxidative deoxyribonucleic acid damage and post-stroke depression (PSD) remains unelucidated.Patients and methodsTwo hundred forty-one first-ever ischemic stroke patients were consecutively recruited within the first 24 h of stroke onset and were followed up at 1 month. Serum 8-hydroxy-2′-deoxyguanosine (8-OHdG) and catalase (CAT) levels were measured within 24 h of admission using a commercially available enzyme-linked immunosorbent assay. The 17-item Hamilton Depression Scale was used to evaluate depressive symptoms. Diagnosis of PSD was made in line with the Diagnostic and Statistical Manual of Mental Disorders, 4th edition criteria for depression.ResultsSerum levels of 8-OHdG (P<0.001) and CAT (P=0.025) increased in depressed patients at admission. A positive correlation was found between the 8-OHdG and CAT levels in both the total stroke patients (r=0.320, P<0.001) and the depressed patients (r=0.300, P=0.012). The 8-OHdG levels were positively correlated with the 17-item Hamilton Depression Scale scores (r=0.129, P=0.046) in depressed patients. Multivariate analyses found that 8-OHdG levels ≥200.0 ng/L were independently associated with PSD (odds ratio, 7.477; 95% CI, 3.342–16.289, P<0.001) after adjusting for possible relevant confounders.ConclusionHigher serum 8-OHdG levels at admission were found to be correlated with PSD 1 month after stroke.

Poststroke Depressive Symptoms Are Associated With Increased Oxidative Deoxyribonucleic Acid Damage.

Poststroke depression is independently associated with poor health outcomes, such as increased mortality, disability, anxiety, and lower quality of life. Identifying the potential biomarkers and detailed mechanisms of poststroke depression may improve the effectiveness of therapeutic intervention. In this cross-sectional study, the authors recruited patients with subacute ischemic stroke who were consecutively admitted for neurorehabilitation. Depression was assessed with the Patient Health Questionnaire-9 (PHQ-9), with a cutoff based on a summed-items score of 10. Polysomnography and laboratory tests for oxidative stress and inflammation were arranged. In total, 139 patients (97 men [69.8%] and 42 women [30.2%]; mean age: 63.2 years [±13.4]) with recent ischemic stroke were recruited and divided into two groups based on their depressive symptoms. Body mass index (BMI), the Barthel Index, percentage of antidepressant usage, and percentage of rapid eye movement (REM) sleep differed significantly between the two groups. The PHQ-9 score was significantly correlated with the levels of total antioxidant capacity, C-reactive protein, and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG). Urinary 8-OHdG, a marker of oxidative stress to DNA, remained significantly and positively correlated with PHQ-9 scores after adjusting for BMI, sleep-onset latency, Barthel Index, mean oxyhemoglobin saturation, age, antidepressant usage, and percentage of REM sleep by using multivariate linear regression. Depressive symptoms were related to increased oxidative DNA damage in patients with subacute ischemic stroke. Urinary 8-OHdG may serve as a potential biomarker for poststroke depression. Further longitudinal studies are needed to elucidate the causal relationship between poststroke depression and elevated oxidative stress level.