Oxidative Deoxyribonucleic Acid Damage Research Articles

Theoretical Study on The Effect of Metal Ions on The Structural Properties of Base

Metal ions play an important role in living organisms, for example Mg2+ is a cofactor for many biological enzymes (including DNA and RNA synthesis), Ca2+ is an important component of bone composition, and metal ions such as Fe, Co, Zn, Ni and Cu also play an important role in the normal functioning of living organisms. One of the main targets of metal ions in living organisms is deoxyribonucleic acid (DNA), which is an important carrier of information stored and transmitted by organisms. The direct interaction between DNA base pairs and metal ions have a significant impact on the structure and function of DNA base pairs, which is demonstrated as following: the binding of metals to bases usually breaks the hydrogen bonds of the base pairs. The N7 atom of a purine residue or the N3 atom of a pyrimidine residue, as well as the outer ring O atom and the phosphate oxygen atom, are the preferred sites for metal binding. The binding of metals to DNA and RNA also indirectly affects the conformation of the sugar ring. REDOX active metal ions have the ability to bind to DNA and can mediate oxidative DNA damage by reacting with endogenous oxidants. According to studies of antioxidants in the field of metal-mediated oxidative DNA damage, metal ion coordination also plays a key role in the mechanism of some antioxidants. Also, metal-DNA interactions are the basis for many anti-cancer drugs, anti-viral drugs and anti-bacterial agents. Metal-mediated oxidative DNA damage is associated with a variety of diseases and conditions, and understanding the binding interactions and subsequent reactivity can facilitate the management or prevention of oxidative damage. It can be seen that the study of the effect of metal ions on the structural properties of DNA bases has far-reaching implications, providing a theoretical basis for the development of novel anticancer drugs, DNA-based metal nanodevice technologies and the fabrication of spectroscopic and reactive probes.

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.

Atomic layer deposited zinc oxide thin film on pencil graphite for DNA sensor applications

Atomic Layer Deposition (ALD) enables precise thin-film deposition on electrode substrates for electrochemical sensors. In this work, we present the first example of ALD grown zinc oxide (ZnO) deposition on pencil graphite surfaces for deoxyribonucleic acid (DNA) sensory applications, including its detection and DNA damage investigation. For DNA sensing studies, the use of highly productive materials is essential. In this context, the ZnO modified pencil graphite electrodes (ZnO/PGEs) exhibited good electrochemical properties that make them a suitable substrate. ZnO films were characterized using scanning electron microscopy (SEM), ultraviolet-visible (UV-Vis) spectroscopy, photoluminescence (PL), X-ray photoelectron spectroscopy (XPS), and electrochemical methods. The DNA recognition capability of the thin film coated electrodes was tested by using differential pulse voltammetry (DPV), which showed a linear response ranging from 1 mg L−1 to 200 mg L−1 based on the oxidation of guanine (G) with a limit of detection value (LOD) of 0.53 mg L−1 (n = 3). In addition to this, impedimetric monitoring of oxidative DNA damage was performed in the presence of copper(II)/hydrogen peroxide (Cu(II)/H2O2) reagents, and protection studies were conducted in the presence of ascorbic acid. ZnO thin film-based electrodes exhibited good sensor performance in terms of sensitivity, stability, and reproducibility.

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.

Voltammetric Measurement of Antioxidant Activity by Prevention of Cu(II)-Induced Oxidative Damage on DNA Bases Using a Modified Electrode.

The protective effect of antioxidants using electrochemical techniques can be evaluated by examining the oxidative changes in deoxyribonucleic acid (DNA) nucleobases. In this study, a gold nanoparticle (AuNP)-decorated and multiwalled carbon nanotube (MWCNT)-Nafion-modified glassy carbon electrode (GCE/AuNP/MWCNT-Nafion) was developed to evaluate the preventive ability of antioxidants on oxidative DNA damage. A modified working electrode was prepared and characterized by cyclic voltammetry, electrochemical impedance spectroscopy, and scanning electron microscopy. The developed electrochemical method relies on two phenomena: (i) reactive species (RS) produced by dissolved oxygen in the presence of copper(II) partially damage the DNA immobilized on the electrode surface and (ii) antioxidant compounds prevent this damage by scavenging the formed RS. Changes in guanine, adenine, and cytosine oxidation signals resulting from DNA damage were measured using differential pulse stripping voltammetry before/after the interaction of dsDNA with Cu(II) while antioxidants were absent or present. The DNA protective ability of antioxidants was assessed for a number of antioxidant compounds (i.e., ascorbic acid, gallic acid, epicatechin, catechin, epicatechin gallate, glutathione, chlorogenic acid, N-acetyl cysteine, rosmarinic acid, quercetin, and rutin). Quercetin was found to show the highest antioxidant effect, and its limit of detection was determined as 1 μM. The manufactured biosensor was put in an application for the determination of antioxidant activity of herbal teas.

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.

Human hair rich in pyridinic nitrogen-base DNA biosensor for direct electrochemical monitoring of palbociclib-DNA interaction

Carbon material derived from the waste-based biomass human hair (H), which is naturally rich in pyridinic nitrogen, provides a significant benefit in biosensor applications with its dominant conductivity character. The carbon material was synthesized from human hair waste by the hydrothermal carbonization (HTC) method, which is a promising green synthesis. A morphological characterization of the carbon materials was performed. In this study, H and amine-functionalized multi-walled carbon nanotubes (NH2-MWCNT) were combined for the first time as a modifier, which enhanced the glassy carbon electrode (GCE) surface area for deoxyribonucleic acid (DNA) biosensor studies. Palbociclib (PLB) is clinically used in the treatment of breast cancer. The novel electrochemical nanobiosensor was used to investigate the dsDNA-PLB interaction to evaluate the possibility that PLB causes conformational changes in DNA structure and/or oxidative damage. The interaction was conducted based on the voltammetric signals of deoxyguanosine (dGuo) and deoxyadenosine (dAdo) by differential pulse voltammetry (DPV) on a bare and H + NH2-MWCNT modified GCE. The proposed analytical method was applied to a pharmaceutical dosage form with a satisfactory recovery of 98.25 %. The nanobiosensor was tested in the presence of some interfering agents. The binding mechanism of dsDNA-PLB was also evaluated by spectroscopic and theoretical calculations.

Evaluation of oxidative stress and mitochondrial function in a type II mucopolysaccharidosis cellular model: in vitro effects of genistein and coenzyme Q10.

Mucopolysaccharidosis type II (MPS II or Hunter Syndrome) is a lysosomal disease caused by deficient degradation of glycosaminoglycans (GAGs) heparan sulfate and dermatan sulfate due to the deficiency of the enzyme iduronate-2-sulfatase. The main treatment for MPS II is the administration of the recombinant form of the enzyme, in a process known as enzyme replacement therapy (ERT). Oxidative damage can contribute to the pathophysiology of MPS II and treatment with ERT can reduce the effects of oxidative stress. For a better understanding of pathophysiology of MPS II, we evaluated biomarkers of mitochondrial dysfunction, DNA (Deoxyribonucleic acid) damage, antioxidant defenses, reactive species production and lysosomal size in IDS-deficient HEK 293 cells and investigate the in vitro effect of genistein and coenzyme Q10 (CoQ) on these biomarkers. An increase in the production of reactive species was demonstrated, as well as an increase in the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). Also, an increase in lysosomal volume and oxidative damage to DNA were verified. There was no evidence of a change in mitochondrial function in this cell model. In the HEK 293 (human embryonic kidney 293) knockout (KO) HP10 cell model we found that genistein at concentrations of 25 and 50μm decreased in vitro the production of reactive species and the activity of the SOD enzyme, showing an antioxidant protective effect. Still, in these cells we verified that the coenzyme Q10 in the concentrations of 5 and 10μm decreased in vitro the activity of the SOD enzyme and in the concentration of 10μm decreased in vitro the DNA damage, also demonstrating antioxidant protection. In conclusion, MPS II knockout cells demonstrated oxidative stress and DNA damage and genistein, as well as coenzyme Q10, have been shown to have an important protective effect in vitro against these oxidative damages.

Association between lead exposure and DNA damage (genotoxicity): systematic review and meta-analysis

Studies suggest that chronic lead (Pb) exposure may induce deoxyribonucleic acid (DNA) damage. However, there is no synthesised evidence in this regard. We systematically reviewed existing literature and synthesised evidence on the association between chronic Pb exposure and markers of genotoxicity. Observational studies reporting biomarkers of DNA damage among occupationally Pb-exposed and unexposed controls were systematically searched from PubMed, Scopus and Embase databases from inception to January 2022. The markers included were micronucleus frequency (MN), chromosomal aberrations, comet assay, and 8-hydroxy-deoxyguanosine. During the execution of thisreview, we followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Mean differences in the biological markers of DNA damage between Pb-exposed and control groups were pooled using the random-effects model. The heterogeneity was assessed using the Cochran-Q test and I2 statistic. The review included forty-five studies comparing markers of DNA damage between Pb-exposed and unexposed. The primary studies utilised buccal and/or peripheral leukocytes for evaluating the DNA damage. The pooled quantitative results revealed significantly higher DNA damage characterised by increased levels of MN and SCE frequency, chromosomal aberrations, and oxidative DNA damage (comet assay and 8-OHdG) among Pb-exposed than the unexposed. However, studies included in the review exhibited high levels of heterogeneity among the studies. Chronic Pb exposure is associated with DNA damage. However, high-quality, multicentred studies are required to strengthen present observations and further understand the Pb's role in inducing DNA damage. CRD42022286810.

8- Hydroxy-Deoxyguanosine (8-OhDG) urine as a biomarker of oxidative damage in late elderly diabetes mellitus

Diabetes Mellitus (DM) is a chronic metabolic disease characterized by high blood sugar levels that exceed normal limits. The DM pathomechanism involves oxidative stress, which has the potential to cause damage to cell components, including Deoxyribonucleic Acid (DNA). 8-hydroxy-deoxyguanosine (8-OhDG) is the most frequently detected oxidative DNA lesion. It is water-soluble and excreted in the urine. This study aimed to compare urine 8-OhDG levels in patients with controlled and uncontrolled blood sugar diabetes and healthy controls aged 56-65 years. Analytical descriptive research with a cross-sectional study design involved 80 participants determined with purposive sampling. The levels of 8-OhDG were measured using the Enzyme-Linked Immunosorbent Assay (ELISA) method. The results showed that urine 8-OhDG levels in DM patients (1.426±0.204ng/mL) were higher than in healthy controls (1.372±0.190ng/mL), although not statistically significant. Urine levels of 8-OhDG in DM patients aged 61-65 years (1.468±0.220ng/mL) were higher than in DM patients aged 56-60 years (1.394±0.190ng/mL), although not statistically significant. Urine levels of 8-Ohdg in controlled DM patient were lower (1.282±0.131 ng/mL) than in uncontrolled DM patient (1.569±0.159 ng/mL), were significantly different (p&lt;0.05). 8-OhDG produced by the body is the final product of oxidative DNA damage.

Curcumin Modulates Nitrosative Stress, Inflammation, and DNA Damage and Protects against Ochratoxin A-Induced Hepatotoxicity and Nephrotoxicity in Rats.

Ochratoxin A (OTA) is a fungal toxin of critical concern for food safety both for human health and several animal species, also representing a cancer threat to humans. Curcumin (CURC) is a natural polyphenol that has anti-apoptotic, anti-inflammatory, and antioxidant effects. The aim of this study was to investigate the cytoprotective effect of CURC against OTA-induced nephrotoxicity and hepatotoxicity through the study of the nitrosative stress, pro-inflammatory cytokines, and deoxyribonucleic acid (DNA) damage. Sprague Dawley rats were daily treated with CURC (100 mg/kg b.w.), OTA (0.5 mg/kg b.w), or CURC with OTA by oral gavage for 14 days. Our results demonstrated that OTA exposure was associated with significant increase of pro-inflammatory and DNA oxidative-damage biomarkers. Moreover, OTA induced the inducible nitric oxide synthase, (iNOS) resulting in increased nitric oxide (NO) levels both in kidney and liver. The co-treatment OTA + CURC counteracted the harmful effects of chronic OTA treatment by regulating inflammation, reducing NO levels and oxidative DNA damage in kidney and liver tissues. Histology revealed that OTA + CURC treatment determinates mainly an Iba1+ macrophagic infiltration with fewer CD3+ T-lymphocytes in the tissues. In conclusion, we evidenced that CURC exerted cytoprotective and antioxidant activities against OTA-induced toxicity in rats.

Occupational exposure to metal-rich particulate matter modifies the expression of repair genes in foundry workers.

Foundry workers are exposed to numerous occupational health hazards, which may result in increased risk of cancer, respiratory disease, and other diseases. Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between multiple occupational exposures in foundry workers and expression of deoxyribonucleic acid (DNA) repair genes as a biomarker of oxidative DNA damage. The study sample comprised 17 foundry workers and 27 matched control subjects. Expression of 8-oxoguanine DNA glycosylase-1 (OGG1), inosine triphosphate pyrophosphate (ITPA), and MutT homolog 1 (MTH1) in peripheral blood was examined using the real-time polymerase chain reaction method. Air sampling to determine exposure to metal-rich particulate matter and measurement of extremely low-frequency electromagnetic fields (ELF-EMFs) were conducted according to the National Institute for Occupational Safety and Health standard methods. Personal air sampling revealed that occupational exposure to particulate matter exceeded the threshold limit values (TLVs) in 76% of the workstations, whereas ELF-EMF exposure appeared to be lower than the TLV. ITPA was significantly upregulated in foundry workers compared with control subjects, whereas no significant difference was observed for OGG1 and MTH1. Moreover, ITPA was strongly and positively correlated with the concentration of metal-rich particulate matter in foundry workers. No significant correlation was found between ELF-EMF exposure and expression of DNA repair genes. DNA repair gene expression may be a sensitive biomarker for occupational exposures, which suggests an involvement of oxidative stress in metal-induced toxicity. Further studies are needed to determine the role of DNA repair gene expression in response to occupational/environmental hazards.

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.

Redox Mechanism of Azathioprine and Its Interaction with DNA.

The electrochemical behavior and the interaction of the immunosuppressive drug azathioprine (AZA) with deoxyribonucleic acid (DNA) were investigated using voltammetric techniques, mass spectrometry (MS), and scanning electron microscopy (SEM). The redox mechanism of AZA on glassy carbon (GC) was investigated using cyclic and differential pulse (DP) voltammetry. It was proven that the electroactive center of AZA is the nitro group and its reduction mechanism is a diffusion-controlled process, which occurs in consecutive steps with formation of electroactive products and involves the transfer of electrons and protons. A redox mechanism was proposed and the interaction of AZA with DNA was also investigated. Morphological characterization of the DNA film on the electrode surface before and after interaction with AZA was performed using scanning electron microscopy. An electrochemical DNA biosensor was employed to study the interactions between AZA and DNA with different concentrations, incubation times, and applied potential values. It was shown that the reduction of AZA molecules bound to the DNA layer induces structural changes of the DNA double strands and oxidative damage, which were recognized through the occurrence of the 8-oxo-deoxyguanosine oxidation peak. Mass spectrometry investigation of the DNA film before and after interaction with AZA also demonstrated the formation of AZA adducts with purine bases.

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.

DNA Electrochemical Biosensors for In Situ Probing of Pharmaceutical Drug Oxidative DNA Damage.

Deoxyribonucleic acid (DNA) electrochemical biosensors are devices that incorporate immobilized DNA as a molecular recognition element on the electrode surface, and enable probing in situ the oxidative DNA damage. A wide range of DNA electrochemical biosensor analytical and biotechnological applications in pharmacology are foreseen, due to their ability to determine in situ and in real-time the DNA interaction mechanisms with pharmaceutical drugs, as well as with their degradation products, redox reaction products, and metabolites, and due to their capacity to achieve quantitative electroanalytical evaluation of the drugs, with high sensitivity, short time of analysis, and low cost. This review presents the design and applications of label-free DNA electrochemical biosensors that use DNA direct electrochemical oxidation to detect oxidative DNA damage. The DNA electrochemical biosensor development, from the viewpoint of electrochemical and atomic force microscopy (AFM) characterization, and the bottom-up immobilization of DNA nanostructures at the electrode surface, are described. Applications of DNA electrochemical biosensors that enable the label-free detection of DNA interactions with pharmaceutical compounds, such as acridine derivatives, alkaloids, alkylating agents, alkylphosphocholines, antibiotics, antimetabolites, kinase inhibitors, immunomodulatory agents, metal complexes, nucleoside analogs, and phenolic compounds, which can be used in drug analysis and drug discovery, and may lead to future screening systems, are reviewed.

DNA and RNA oxidative damage are associated to mortality in patients with cerebral infarction

ObjectiveSecondary injury due to oxidation may occur during ischemic stroke, possibly leading to oxidative damage to deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). Higher blood concentrations of 8-hydroxy-2′-deoxyguanosine (8-OHdG) (through the oxidation of guanosine from DNA) have been found in ischemic stroke patients than in healthy subjects, and in patients with versus without post-ischemic stroke depression. The present study was carried out to explore the possible association between serum DNA and RNA oxidative damage and mortality in patients with cerebral infarction. MethodsA prospective, multicenter observational study was carried out in the Intensive Care Units of 6 Spanish hospitals. We included patients with severe malignant middle cerebral artery infarction (MMCAI) defined as ischemic changes evidenced by computed tomography in more than 50% of the middle cerebral artery territory and a Glasgow Coma Score (GCS)<9. Serum concentrations of the three oxidized guanine species (OGS) (8-hydroxyguanine from DNA or RNA, 8-hydroxyguanosine from RNA, and 8-OHdG from DNA) on the day of MMCAI diagnosis were determined. The study endpoint was 30-day mortality. ResultsWe found higher serum OGS levels (p<0.001) in non-surviving (n=34) than in surviving patients (n=34). Logistic regression analyses showed serum OGS levels to be associated to 30-day mortality controlling for lactic acid, GCS and platelet count (OR=1.568; 95%CI=1.131–2.174; p=0.01). ConclusionsThe novel observation in this study is the association between global serum OGS concentration and mortality in ischemic stroke patients.