The impact of OGG1, MTH1 and MnSOD gene polymorphisms on 8-hydroxy-2′-deoxyguanosine and cellular superoxide dismutase activity in myocardial ischemia–reperfusion

2010 ◽  
Vol 38 (4) ◽  
pp. 2427-2435 ◽  
Author(s):  
Bensu Karahalil ◽  
Elvin Kesimci ◽  
Esra Emerce ◽  
Tulin Gumus ◽  
Orhan Kanbak
Keyword(s):  
Superoxide Dismutase ◽  
Myocardial Ischemia ◽  
Gene Polymorphisms ◽  
Ischemia Reperfusion ◽  
Superoxide Dismutase Activity ◽  
Myocardial Ischemia Reperfusion ◽  
The Impact ◽  
Mnsod Gene

scholarly journals Relationship between Superoxide Dismutase Manganese Gene Polymorphism and Eye Tumors

2021 ◽  
Vol 9 (A) ◽  
pp. 229-232
Author(s):  
Rodiah Rahmawaty Lubis ◽  
Cut Adeya Adella ◽  
Lokot Donna Lubis
Keyword(s):  
Superoxide Dismutase ◽  
Gene Polymorphism ◽  
Gene Polymorphisms ◽  
Cancer Biology ◽  
Orbital Tumor ◽  
Control Group ◽  
Orbital Tumors ◽  
The Impact ◽  
The Relationship ◽  
Mnsod Gene

ABSTRACT   Background: Orbital tumor in Indonesia is one of the eye health problems that can cause blindness. The impact caused by orbital tumors on patients is quite large because it can result in blindness and even death due to its metastatic nature. The role that SOD plays in cancer biology is not well understood, most studies showing a more oxidative state, characterized by increased intracellular ROS, particularly superoxide. Objective: To determine the relationship between Manganese Superoxide Dismutase (SOD2) gene polymorphisms and the incidence of orbital tumors in Medan. Methods: This study is an analytic observational study with a cross-sectional data collection method using controls. Comparisons were made between the control group and the observed group to see the relationship between SOD2 polymorphisms and the risk of orbital tumor incidence in Medan. The ophthalmic examination, anterior and posterior segments, and assessment of CT orbit if deemed necessary for the orbital tumor patients. Histopathological examination was done by the Pathologist. Blood samples was taken for polymorphism examination on extracted DNA using the Polymerase Chain Reaction (PCR) and Restriction Fragment Length Polymorphism (RFLP) methods. Results: About 30 patients that met the inclusion criterias. Laterality, the left eye is more likely to suffer from tumors when compared to the right eye. This study found as many as 16 patients, while malignant tumors was 14 patients. There was a relationship between the MnSOD gene polymorphism and the incidence of orbital tumors (p <0.001), there was a relationship between the MnSOD gene polymorphism and the incidence of orbital tumors in the female sex (p <0.001) Conclusion: There was a relationship between MnSOD gene polymorphisms and the incidence of orbital tumors (p <0.001)

Effects of Morphine Postconditioning on Myocardial Ischemia-Reperfusion Injury in Rats In Vivo

2013 ◽  
Vol 680 ◽  
pp. 617-619 ◽  
Author(s):  
Da Peng Gao ◽  
Guo Qing Zhao ◽  
Jia Wang ◽  
Ming Gao
Keyword(s):  
Superoxide Dismutase ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Group I ◽  
Cardiac Apoptosis ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective.To investigate the effects of morphine postconditioning on Myocardial ischemia reperfusion injury in rats in vivo. Methods. To randomly divide 40 male SD rats equally into 4 groups, including Sham group in which the chest was opened without ligating the left coronary artery, ischemia-reperfusion group(Group I/R ), ischemic preconditioning group(Group IPC ) and morphine postconditioning group(GroupMOR) in which 0. 3 mg/kg morphine was given intravenously 5 min before reperfusion. The left anterior descending coronary arterys(LAD) of rats in five groups are ligated for 30 minutes and are re-perfused for 90 minutes. Cardiac Apoptosis was determined quantitatively by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） methods． To calculate the concentration of the serum malondialdehyde(MDA) with Thiobarbituric acid (TBA) reaction method and the activity of the superoxide dismutase (SOD) with xanthine oxidase reaction method. Result. Comparing with Group S, the quantity of the cardiac apoptosis in Group I/R, IPC and MOR rised in different levels. Comparing with Group 1/R, the quantity of the cardiac apoptosis in Group IPC and MOR reduced obviously. Comparing with Group 1/R, the concentration of the serum malondialdehyde (MDA) in the other four groups all reduced and the activity of the superoxide dismutase increased. Conclusion. Morphine postconditioning can significantly reduce myocardial apoptosis induced by ischemia-reperfusion injury，reduce myocardial infarct size, decrease the concentration of MDA, and increase the activity of SOD. Therefore, morphine postconditioning has protective effects on myocardial ischemia-reperfusion injury in rats in vivo. Morphine is a potent kind of opioid analgesics, which is widely used in clinical anesthesia. However, further studies are needed on effects of morphine postconditioning on myocardial ischemia reperfusion injury. In order to provide the foundations for clinical application, the authors investigate the effects of morphine postconditioning on myocardial ischemia reperfusion injury through comparison and analysis of the cardiac apoptosis, the concentration of the serum malondialdehyde (MDA) and the activity of the superoxide dismutase (SOD) in Group S, I/R, IPC and MOR.

Abstract 13565: Superoxide Dismutase-loaded Nanoparticles Attenuate Myocardial Ischemia-Reperfusion Injury and Protect Against Chronic Adverse Ventricular Remodeling

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Peter J Altshuler ◽  
Zhiliang J Cheng ◽  
Alexis R Schiazza ◽  
Mark R Helmers ◽  
Robin Hu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ventricular Remodeling ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Injury ◽  
Chronic Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Enzyme Retention

Introduction: Revascularization relieves myocardial ischemia but induces additional reperfusion injury by oxidative stress. Superoxide dismutase (SOD) is a potent antioxidant with preclinical promise in reducing reperfusion injury but is not well retained within the myocardium. Hypothesis: Use of SOD-encapsulated nanoparticles (NP-SOD) will improve SOD retention and preserve cardiac function in a rat model of myocardial ischemia-reperfusion (I/R) injury. Methods: Ischemia was maintained for 60 minutes via occlusion of the left anterior descending artery (LAD). Immediately prior to reperfusion, intramyocardial injections of NP-SOD, free SOD or phosphate buffered saline (PBS) were administered along the border of ischemic myocardium. Acute injury was assessed 3 hours post-reperfusion (n=8 per group), and chronic injury at 4 weeks (n=12). Hemodynamics were measured by echocardiography and pressure-volume loops. Acute and chronic injury were examined histologically. Protein isolates at 3 hours measured mediators of cell-death. Intramyocardial enzyme retention analysis was performed by injecting NP or free fluorescent-tagged SOD and explanting hearts for imaging at 0, 24 and 72 hours (n=4 per group). Results: Intramyocardial SOD retention was 25% greater in NP-SOD than free SOD at 24 hours (p<0.01) and 78% greater at 72 hours (p<0.01). NP-SOD exhibited improved ventricular function by ejection fraction at 4 weeks (64%) compared to free SOD (51%; p<0.01) and PBS (43%; p<0.01). Cardiac output, stroke volume and end-systolic elastance were greater in NP-SOD. Histology at 28 days demonstrated 54% less macroscopic fibrosis and 85% less microscopic collagen deposition in NP-SOD compared to PBS, and 33/79% compared to free SOD (all p<0.05). Quantifying RIPK3 protein levels in ‘at risk’ myocardium at 3 hours demonstrated 2.5-fold reduced upstream necrosome activation. Conclusions: NP-SOD provides prolonged enzyme retention within the myocardium. Intramyocardial NP-SOD administration prior to reperfusion attenuates acute myocardial injury and protects against chronic adverse ventricular remodeling. SOD acts by downregulating necrosis. These findings suggest potential for NP-SOD based therapy in mitigating myocardial I/R injury.

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