MEASUREMENT OF DNA DAMAGE, OXIDATIVE STRESS, AND GENE EXPRESSION OF β-CATENIN AND P53 GENES IN LIVER AND BRAIN OF MALE MICE RECEIVING MONOSODIUM L-GLUTAMATE MONOHYDRATE

Introduction: Monosodium L-glutamate (MSG) monohydrate is a widespread nutritional additive and flavoring agent frequently consumed all over the world. In this study, we investigate the action of daily oral intake of MSG monohydrate in vivo using mammalian systems. Methods: Mice divided as follows: Group I (normal control), Group II, and Group III treated with MSG for 2 and 4 weeks, respectively. Brain and liver dissected out for the detection of fragmented DNA, DNA damage, and assay of oxidative stress markers. Moreover, expression levels of ß-Cat and p53 genes were measured by a real-time quantitative polymerase chain reaction. Results: The results showed a significant difference in MSG-treated group at the 2-time intervals than the control one regarding parameters of oxidative stress, and these were accompanied by a significant decline in glutathione (GSH) and a ratio of oxidized and reduced GSH in both tissues. Significant elevation of laddered DNA and oxidative DNA damage was observed in groups treated with MSG. In addition, a significant decline in gene expression of ß-Catenin in liver and brain tissues with elevations in the gene expression of p53 in the brain. Furthermore, the p53 gene in liver tissue was significantly upregulated in mice administered MSG for 15 days and was downregulated after 30 days of MSG intake compared with the control. Conclusion: According to our results, oral consumption of MSG leads to oxidative stress-mediated DNA damage and apoptosis.

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Oxidative lipid, protein, and DNA damage as oxidative stress markers in vascular complications of diabetes mellitus

Clinical & Investigative Medicine ◽

10.25011/cim.v34i3.15189 ◽

2011 ◽

Vol 34 (3) ◽

pp. 163 ◽

Cited By ~ 71

Author(s):

Omur Tabak ◽

Remise Gelisgen ◽

Hayriye Erman ◽

Fusun Erdenen ◽

Cüneyt Muderrisoglu ◽

...

Keyword(s):

Oxidative Stress ◽

Diabetes Mellitus ◽

Dna Damage ◽

Oxidative Dna Damage ◽

Vascular Complications ◽

Diabetic Group ◽

Control Group ◽

Diabetic Patients ◽

Serum Samples ◽

Type 2 Diabetic Patients

Purpose: The purpose of this study was to determine the effects of diabetic complications on oxidation of proteins, lipids, and DNA and to investigate the relationship between oxidative damage markers and clinical parameters. Methods: The study group consisted of 69 type 2 diabetic patients (20 patients without complication, 49 patients with complication) who attended internal medicine outpatient clinics of Istanbul Education and Research Hospital and 19 healthy control subjects. In serum samples of both diabetic patients and healthy subjects, 8-hydroxy-2’deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, Nε-(hexanoyl)lysine (HEL) and 15-F2t-iso-prostaglandin (15-F2t-IsoP). as products of lipooxidative damage, advanced oxidation protein products (AOPP), as markers of protein damage, and paraoxonase1 (PON1) as antioxidant were studied. Results: 15-F2t-IsoP (p < 0.005) and AOPP (p < 0.001) levels were significantly higher in diabetic group than control group while there were no significant differences in levels of 8-OHdG and HEL between the two groups. AOPP (p < 0.001) and 8-OHdG (p < 0.001) were significantly higher in diabetic group with complications compared to diabetic group without complications. Conclusions: Increased formation of free radicals and oxidative stress, under conditions of hyperglycaemia, is one of the probable causes for evolution of complications in diabetes mellitus. Our study supports the hypothesis that oxidant/antioxidant balance is disturbed in diabetic patients.

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Investigating the Effect of Fresh Frozen Plasma and Albumin on DNA Damage and Oxidative Stress Biomarkers in Poisoning Cases by Organophosphates

Drug Research ◽

10.1055/a-1261-9151 ◽

2020 ◽

Vol 71 (01) ◽

pp. 10-16

Author(s):

Saeed Afzali ◽

Manoochehr Karami ◽

Nejat Kheyripour ◽

Akram Ranjbar

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Fresh Frozen Plasma ◽

Adjunctive Treatment ◽

Control Group ◽

Oxidative Stress Biomarkers ◽

Significant Difference ◽

Antioxidant Parameters ◽

Fresh Frozen ◽

Frozen Plasma

AbstractThe efficacy of albumin and fresh frozen plasma (FFP) and their effects on biomarkers of oxidative stress has been evaluated. In a randomized clinical control trial, 33 poisoned patients by Organophosphate (OP) were enrolled in the research and divided into three groups. The first group underwent conventional treatments by atropine and pralidoxime (control group); the second and third groups, in addition to traditional treatments, received albumin and FFP. Cholinesterase (ChE) enzyme activity, total antioxidant capacity (TAC), serum thiol groups (TTG), malonyl aldehyde (MDA) and DNA damage were measured in all treatment and control groups. Patients were matched in terms of demographic characteristics at the beginning of the study. ChE activity was increased in all three groups during treatment, which was more noticeable in the FFP group and was statistically significant in both albumin and FFP group compared to the control group (p<0.05). TAC increased, and TTG decreased in FFP and albumin groups compared to the control group; no significant difference was observed. MDA decreased in albumin and FFP and was significantly different in the FFP group compared to the control group (p<0.05). The amount of DNA damage in FFP and albumin groups decreased, and there was a significant difference compared to the control group (p<0.05). According to the results of this study, due to the decrease of oxidative damage parameters and the increase of antioxidant parameters in albumin and specially FFP groups, FFP may be considered as an adjunctive treatment for OP poisoning.

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In-depth comparative toxicogenomics of glyphosate and Roundup herbicides: histopathology, transcriptome and epigenome signatures, and DNA damage

10.1101/2021.04.12.439463 ◽

2021 ◽

Author(s):

Robin Mesnage ◽

Mariam Ibragim ◽

Daniele Mandrioli ◽

Laura Falcioni ◽

Fiorella Belpoggi ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Dna Methylation ◽

European Union ◽

Dna Damage ◽

Protein Misfolding ◽

Control Group ◽

The European Union ◽

Dna Methylation Profiling ◽

Methylation Profiling

Background. Health effects from exposure to glyphosate-based herbicides is an intense matter of debate. Toxicity including genotoxicity of glyphosate alone has been repeatedly tested over the last 40 years. Contrastingly, few studies have conducted comparative investigations between glyphosate and its commercial herbicide formulations, such as Roundup. We thus performed the first in-depth comparative toxicogenomic evaluation of glyphosate and a typical European Union Roundup formulation by determining alterations in transcriptome and epigenome profiles. Methods. Glyphosate and the European Union reference commercial formulation Roundup MON 52276 (both at 0.5, 50, 175 mg/kg bw/day glyphosate equivalent concentration) were administered to rats in a subchronic 90-day toxicity study. Standard clinical biochemistry and kidney and liver histopathology was performed. In addition, transcriptomics and DNA methylation profiling of liver and selective gene expression analysis of kidneys was conducted. Furthermore, a panel of six mouse embryonic reporter stem cell lines validated to identify carcinogenic outcomes (DNA damage, oxidative stress, and protein misfolding) were used to provide insight into the mechanisms underlying the toxicity of glyphosate and 3 Roundup formulations. Results. Histopathology and serum biochemistry analysis showed that MON 52276 but not glyphosate treatment was associated with a statistically significant increase in hepatic steatosis and necrosis. Similar lesions were also present in the liver of glyphosate-treated groups but not in the control group. MON 52276 altered the expression of 96 genes in liver, with the most affected biological functions being TP53 activation by DNA damage and oxidative stress as well as the regulation of circadian rhythms. The most affected genes in liver also had their expression similarly altered in kidneys. DNA methylation profiling of liver revealed 5,727 and 4,496 differentially methylated CpG sites between the control group and the group of rats exposed to glyphosate and MON 52276, respectively. Direct DNA damage measurement by apurinic/apyrimidinic lesion formation in liver was increased with glyphosate exposure. Mechanistic evaluations showed that two Roundup herbicides but not glyphosate activated oxidative stress and misfolded protein responses. Conclusions. Taken together, the results of our study show that Roundup herbicides are more toxic than glyphosate, activating mechanisms involved in cellular carcinogenesis and causing gene expression changes reflecting DNA damage. This further highlights the power of high-throughput omics methods to detect metabolic changes, which would be missed by relying solely on conventional biochemical and histopathological measurements. Our study paves the way for future investigations by reporting a panel of gene expression changes and DNA methylation sites, which can serve as biomarkers and potential predictors of negative health outcomes resulting from exposure to glyphosate-based herbicides.

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Assessment of DNA damage and oxidative stress among traffic conductors and coal miners

Pakistan Journal of Medical Sciences ◽

10.12669/pjms.37.2.2848 ◽

2021 ◽

Vol 37 (2) ◽

Author(s):

Irfan Ullah ◽

Muhammad Zahid ◽

Muhammad Jawad ◽

Aatik Arsh

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Superoxide Dismutase ◽

Tail Length ◽

Control Group ◽

Control Groups ◽

Coal Miners ◽

Significant Difference ◽

And Oxidative Stress ◽

Mine Workers

Objective: To assess the DNA damage and oxidative stress among traffic conductors and coal miners. Methods: An analytical cross-sectional survey was conducted in Karak, Pakistan from March to October 2019. A total of 240 individuals participated in the study with an age range between 17 to 55 years. Among the total sample, 60 participants had exposure to traffic pollution while 60 were mine workers. Two control groups, consisting of 60 individuals each, were also recruited for comparison with the two exposure groups. Comet assay protocols were performed for assessing DNA damage and oxidative stress (length of DNA tail, levels of Superoxide Dismutase (SOD), Malondialdehyde (MDA) and Glutathione (GSH)). Data was analyzed using T-test on statistix 9.0 software. Results: The DNA tail length in traffic conductors ranged from 26.83-30.55µm (Mean=28.69 µm while their control group had DNA tail length of 7.98-9.26µm (Mean= 8.62). There was significant difference (P <0.001) between exposure and control group. The DNA length recorded in coal mine workers and their control group was ranged from 29.06-31.26µm (Mean=30.16µm) and 9.42-10.22µm (Mean=9.82), respectively. There was significant difference (P <0.001) between the two groups. As compared to control groups, both exposure groups have high levels of Superoxide Dismutase and Malondialdehyde and low levels of Glutathione. The finding was statistically significant (P <0.001). Conclusion: Increased inhalational exposure to air pollutants via working in traffic or coal mines can impose higher oxidative stress and DNA damage among workers as compared to the general population. doi: https://doi.org/10.12669/pjms.37.2.2848 How to cite this:Ullah I, Zahid M, Jawad M, Arsh A. Assessment of DNA damage and oxidative stress among traffic conductors and coal miners. Pak J Med Sci. 2021;37(2):---------. doi: https://doi.org/10.12669/pjms.37.2.2848 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Vitamin D attenuates gentamicin-induced acute renal damage via prevention of oxidative stress and DNA damage

Human & Experimental Toxicology ◽

10.1177/0960327118812166 ◽

2018 ◽

Vol 38 (3) ◽

pp. 321-335 ◽

Cited By ~ 5

Author(s):

MA Mohammed ◽

BE Aboulhoda ◽

RH Mahmoud

Keyword(s):

Oxidative Stress ◽

Vitamin D ◽

Dna Damage ◽

Kidney Function ◽

Control Group ◽

Albino Rats ◽

Nuclear Factor ◽

Group I ◽

First Choice ◽

Depth Analysis

Background: Despite being one of the most nephrotoxic drugs, gentamicin (GM) remains a mainstay as a first-choice agent in a vast variety of clinical situations owing to its superlative efficiency as a broad-spectrum antibiotic in treating several life-threatening bacterial infections. This urgently calls for the need for in-depth analysis of the mechanisms governing GM-induced nephrotoxicity and entails the necessity of presenting novel protective agents capable of ameliorating those renal deleterious effects. The reactive oxygen species and redox-sensitive transcription factors in GM-induced nephrotoxicity have recently called attention. Purpose: This study has been designed to shed light on the possible mechanisms of GM-induced nephrotoxicity and to provide a consensus set of histopathological, immunohistochemical, genetic and biochemical parameters elucidating the protective role of vitamin D against this nephrotoxicity. Methods: Twenty-four adult male albino rats were equally divided into four groups: group I (control group), group II (GM), group III (GM + vitamin D) and group IV (vitamin D only). Kidney function tests, histopathological examination, gene expression of nuclear factor 2, nuclear factor kappa beta (NF-κB) and western blot of NF-κB p65, assessment of glutathione peroxidase and nicotinamide adenine dinucleotide phosphate oxidase (NADPH) oxidase by ELISA, as well as immunohistochemical evaluation of inducible nitric oxide, malondialdehyde, 8-hydroxy 2 deoxyguanine and vitamin D receptor, have been carried out. Results: The kidney function deterioration, tissue oxidative stress development and the histopathological changes induced by GM were significantly attenuated by vitamin D administration. Conclusion: Vitamin D attenuates GM nephrotoxicity through its antioxidant properties and prevention of DNA damage.

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Resveratrol Reverses Thioacetamide-Induced Renal Assault with respect to Oxidative Stress, Renal Function, DNA Damage, and Cytokine Release in Wistar Rats

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/1702959 ◽

2019 ◽

Vol 2019 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

Seema Zargar ◽

Mona Alonazi ◽

Humaira Rizwana ◽

Tanveer A. Wani

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Dna Damage ◽

Creatine Kinase ◽

Renal Function ◽

Treated Group ◽

Control Group ◽

Cytokine Release ◽

Kidney Toxicity ◽

Significant Difference

Background. Thioacetamide (TAA), a class 2B-type carcinogen, is a potent toxicant. Toxicities caused by this compound in various tissues due to oxidative stress, increase of proinflammatory markers, and apoptosis have been reported; however, reports on kidney toxicity are negligible. Resveratrol (RSV), on the other hand, has demonstrated antioxidant and anti-inflammatory effects in different cases. Resveratrol’s protective effects against TAA kidney toxicity were investigated in four rat groups. Methodology. Four groups of rats were studied as follows (n=8): control group, where rats were fed normal diet and water; TAA group, where rats received 0.3% TAA in water for two weeks; RSV group, where rats received 10 mg/kg body weight (bw) of RSV as oral suspension for two weeks; and treated group, where rats orally received 10 mg/kg bw RSV and simultaneously received 0.3% TAA for two weeks. Kidney homogenates from all groups were analyzed for cytokine release (IL-4, TNF-α, and IFN-γ) and oxidative stress (lipid peroxidation, catalase, and 8-OHdG). The serum of rats was analyzed for the quantification of renal function markers (blood urea nitrogen (BUN), creatinine, and creatine kinase). Result. A significant increase in the renal function markers (BUN, 240%; creatinine, 187%; and creatine kinase, 117%), oxidative stress parameters (lipid peroxidation, 192% increase; catalase, 30.5% decrease), cytokines (IL-4, 120%; TNF-α, 129%; and IFN-γ, 133%), and DNA damage was observed in the TAA-treated group. All changes were significantly reversed in the group treated with RSV and TAA (P<0.05) in combination, with no significant difference compared to the control group. Conclusion. We conclude that resveratrol shows protection against TAA toxicity in rat kidney with respect to DNA damage, oxidative stress, renal function and cytokine release.

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Reductive regulation of BECN1 gene in adult Egyptian patients with do novo AML

Egyptian Journal of Medical Human Genetics ◽

10.1186/s43042-020-00087-z ◽

2020 ◽

Vol 21 (1) ◽

Author(s):

Manal Fawzy Ghozlan ◽

Botheina Ahmed Thabet Farweez ◽

Nesma Ahmed Safwat ◽

Noha Bassiouny Hassan ◽

Walaa Ali Elsalakawy

Keyword(s):

Gene Expression ◽

Bone Marrow ◽

Peripheral Blood ◽

De Novo ◽

Quantitative Polymerase Chain Reaction ◽

Control Group ◽

Significant Difference ◽

Egyptian Patients ◽

Blast Cells ◽

De Novo Aml

Abstract Background Acute myeloid leukaemia (AML) is a clonal haematopoietic disease characterized by the proliferation of immature blast cells in the bone marrow and peripheral blood. Autophagy is an inherent cellular route by which waste macromolecules are engulfed within autophagosomes prior to their fusion with cytoplasmic lysosomes for degradation. The BECN1 gene encodes the Beclin-1 protein, which regulates autophagy. Few reports have investigated BECN1 gene expression and its value in AML patients. Results This randomized case-control study included 50 newly diagnosed AML patients, in addition to 20 subjects as a control group. BECN1 gene expression was assessed using real-time quantitative polymerase chain reaction (qRT-PCR). The median level of BECN1 gene expression in AML patients was 0.41 (IQR 0.29–1.03) in comparison to 1.12 (IQR 0.93–1.26) in the control group (P = 0.000). Seventy-two percent of AML patients showed reduced BECN1 gene expression, which was highly significantly associated with intermediate and adverse cytogenetic risk. Reduced BECN1 gene expression was associated with older age, higher total leukocyte counts, the presence of peripheral blood blast cells, a higher percentage of bone marrow blast cells, and higher expression of CD34 and CD117. FLT3-ITD mutation was detected in 14 patients (38.9%), all of whom showed reduced BECN1 gene expression (P = 0.006). BECN1 gene expression was also reduced in non-responder AML patients, with a highly statistically significant difference (P = 0.002). Conclusion A reduction in BECN1 gene expression might indicate a poor prognosis in adult Egyptian patients with de novo AML. Decreased BECN1 gene expression is associated with a higher risk of resistance to treatment. Targeting autophagy pathways may help in the treatment of AML patients.

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Oxidative DNA damage and oxidative stress in lead-exposed workers

Human & Experimental Toxicology ◽

10.1177/0960327116665674 ◽

2016 ◽

Vol 36 (7) ◽

pp. 744-754 ◽

Cited By ~ 33

Author(s):

M Dobrakowski ◽

N Pawlas ◽

A Kasperczyk ◽

A Kozłowska ◽

E Olewińska ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oxidative Damage ◽

Oxidative Dna Damage ◽

Blood Lead ◽

Antioxidant Defense System ◽

Control Group ◽

High Exposure ◽

Human Leukocytes ◽

Low Exposure

There are many discrepancies among the results of studies on the genotoxicity of lead. The aim of the study was to explore lead-induced DNA damage, including oxidative damage, in relation to oxidative stress intensity parameters and the antioxidant defense system in human leukocytes. The study population consisted of 100 male workers exposed to lead. According to the blood lead (PbB) levels, they were divided into the following three subgroups: a group with PbB of 20–35 μg/dL (low exposure to lead (LE) group), a group with a PbB of 35–50 µg/dL (medium exposure to lead (ME) group), and a group with a PbB of >50 μg/dL (high exposure to lead (HE) group). The control group consisted of 42 healthy males environmentally exposed to lead (PbB < 10 μg/dL). A comet assay was used to measure the DNA damage in leukocytes. We measured the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) as well as the concentration of malondialdehyde (MDA), and the value of the total antioxidant capacity. The level of PbB was significantly higher in the examined subgroups than in the control group. The percentage of DNA in the tail was significantly higher in the LE, ME, and HE subgroups than in the control group by 10% ( p = 0.001), 15% ( p < 0.001), and 20% ( p < 0.001), respectively. The activity of GR was significantly lower in the LE and ME subgroups than in the control group by 25% ( p = 0.007) and 17% ( p = 0.028), respectively. The activity of G6PD was significantly lower in the ME subgroup by 25% ( p = 0.022), whereas the activity of GST was significantly higher in the HE subgroup by 101% ( p = 0.001) than in the control group. Similarly, the activity of SOD was significantly higher in the LE and ME subgroups by 48% ( p = 0.026) and 34% ( p = 0.002), respectively. The concentration of MDA was significantly higher in the LE, ME, and HE subgroups than in the control group by 43% ( p = 0.016), 57% ( p < 0.001), and 108% ( p < 0.001), respectively. Occupational lead exposure induces DNA damage, including oxidative damage, in human leukocytes. The increase in DNA damage was accompanied by an elevated intensity of oxidative stress.

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Effect of Coal Dust Exposure on the SOD Activity and the Oxidative DNA Damage in Asthmatic Mice

The Indonesian Biomedical Journal ◽

10.18585/inabj.v11i2.579 ◽

2019 ◽

Vol 11 (2) ◽

pp. 159-66

Author(s):

Windy Yuliana Budianto ◽

Husnul Khotimah ◽

Eko Suhartono

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Oxidative Dna Damage ◽

Coal Dust ◽

Negative Control ◽

Dust Exposure ◽

Dust Particles ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Sod Activity

BACKGROUND: Coal dust is known to trigger hypersensitivity and inflammation of the respiratory tract as it increases oxidative stress leading to asthma. To date, the relationship of coal dust exposure in the pathomechanism of asthma remains unclear. This study was aimed to examine the effect of coal dust exposure on the superoxide dismutase (SOD) activity and the oxidative DNA damage indicated by increased serum 8-hydroxy-2' -deoxyguanosine (8-OHdG) in asthmatic mice.METHODS: Twenty-four female balb/c mice were divided into four groups. The first group was the control group. The second group was the negative control group which composed of mice exposed to coal dust particles. The third group was composed of ovalbumin (OVA)-sensitized mice. The fourth group was composed of OVA-sensitized mice and exposed to coal dust particles. The inflammatory process was identified by serum interleukin (IL)-13 concentration using Enzyme-linked Immunosorbent Assay (ELISA) method. Meanwhile, the oxidative stress was examined by measuring the SOD activity using the Nitro Blue Tetrazolium (NBT) method, and the 8-OHdG concentration was quantified by ELISA method.RESULTS: There was an increasing IL-13 in OVAtreated coal dust exposed group along with the increment of 8-OHdG (statistically not significant). SOD activity measured in serum was decreased in all groups (p>0.05). Combination of OVA and coal dust showed the worst effect on IL-13, 8-OHdG and SOD activity.CONCLUSION: Coal dust exposure for four weeks does not adequately induce the oxidative DNA damage in asthmatic mice.KEYWORDS: asthma, coal dust, IL-13, SOD, 8-OHdG

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Abstract 2039: Urinary 8-Hydroxy-2′-Deoxyguanosine Levels Decrease After Cardioversion in Atrial Fibrillation

Circulation ◽

10.1161/circ.116.suppl_16.ii_441-c ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Takashi Uemura ◽

Hiroshige Yamabe ◽

Yasuhiro Nagayoshi ◽

Yasuaki Tanaka ◽

Kenji Morihisa ◽

...

Keyword(s):

Oxidative Stress ◽

Atrial Fibrillation ◽

Dna Damage ◽

Time Course ◽

Oxidative Dna Damage ◽

Enzyme Linked Immunosorbent Assay ◽

Potential Marker ◽

Significant Difference ◽

The Difference ◽

Pharmacological Cardioversion

Background : Atrial fibrillation (AF) has been shown to be associated with increased oxidative stress mediated by reactive oxygen species (ROS). Previous studies have proposed that there is a link between oxidative stress and AF, and thus oxidative stress may contribute to the pathological consequences of AF such as thrombosis, inflammation, and atrial tissue remodeling. Urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) which is a product of deoxyribonucleic acid (DNA) damage by ROS has become to be regarded as a putative biomarker of oxidative DNA damage. Also, biopyrrins which are oxdative metabolites of bilirubin (an important scavenger of ROS) are considered as the potential marker of oxdative stress. In the present study, we assessed serial changes in oxidative stress in patients with AF after cardioversion by measuring urinary 8-OHdG and urinary biopyrrin excretion. Methods and Results : The study subjects consisted of 15 patients with persistent or chronic AF, who underwent electrical or pharmacological cardioversion. We measured urinary 8-OHdG and biopyrrin levels obtained before cardioversion and 24 hours after cardioversion using enzyme-linked immunosorbent assay. There was no significant difference in the biopyrrin/creatinine levels before and 24 hours after cardioversion (3.2±2.6 vs. 3.3±2.4 mU/mg, P=NS). However, 8-OHdG/creatinine levels decreased significantly 24 hours after cardioversion (18.4±9.1 vs. 14.7±8.5 ng/mg, P=0.0012). There was no significant correlation between urinary 8-OHdG/creatinine and biopyrrin/creatinine levels. This discrepancy may be related to the difference in the time course between urinary 8-OHdG/creatinine and biopyrrin/creatinine levels. Thus, measurement of 8-OHdG/creatinine levels seemed to be a more useful marker which reflects the oxidative stress than biopyrrin/creatinine levels at the time 24 hours after cardioversion. Conclusions : These findings suggest that the restoration of sinus rhythm by cardioversion decreases oxidative DNA damage in AF patients, and urinary 8-OHdG may be useful for the estimation of oxidative stress in AF patients. The increase of oxidative stress may play an important role in the pathogenesis of AF, and persist AF and result in the perpetuation of AF.

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