Ischemia/Reperfusion in Diving Birds and Mammals: How they Avoid Oxidative Damage

2011 ◽  
pp. 178-189 ◽  
Author(s):  
Tania Zenteno-Savín ◽  
José Pablo Vázquez-medina ◽  
Nadiezhda Cantú-Medellín ◽  
Paul J. Ponganis ◽  
Robert Elsner
Keyword(s):  
Oxidative Damage ◽  
Ischemia Reperfusion

scholarly journals Alternative Interventions to Prevent Oxidative Damage following Ischemia/Reperfusion

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Simón Quetzalcoatl Rodríguez-Lara ◽  
Ernesto German Cardona-Muñoz ◽  
Ernesto Javier Ramírez-Lizardo ◽  
Sylvia Elena Totsuka-Sutto ◽  
Araceli Castillo-Romero ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Remote Ischemic Preconditioning ◽  
Therapeutic Approaches ◽  
Alternative Interventions ◽  
Stress States ◽  
The Relationship ◽  
Irreparable Damage

Ischemia/reperfusion (I/R) lesions are a phenomenon that occurs in multiple pathological states and results in a series of events that end in irreparable damage that severely affects the recovery and health of patients. The principal therapeutic approaches include preconditioning, postconditioning, and remote ischemic preconditioning, which when used separately do not have a great impact on patient mortality or prognosis. Oxidative stress is known to contribute to the damage caused by I/R; however, there are no pharmacological approaches to limit or prevent this. Here, we explain the relationship between I/R and the oxidative stress process and describe some pharmacological options that may target oxidative stress-states.

Melatonin protects against ischemia/reperfusion-induced oxidative damage to mitochondria in fetal rat brain

2001 ◽  
Vol 31 (2) ◽  
pp. 167-172 ◽  
Author(s):  
A. Wakatsuki ◽  
Y. Okatani ◽  
K. Shinohara ◽  
N. Ikenoue ◽  
T. Fukaya
Keyword(s):  
Oxidative Damage ◽  
Rat Brain ◽  
Ischemia Reperfusion ◽  
Fetal Rat ◽  
Fetal Rat Brain

scholarly journals NLRC5 alleviated OGD/R-induced PC12-cell injury by inhibiting activation of the TLR4/MyD88/NF-κB pathway

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052094045
Author(s):  
Zhen Zhang ◽  
Yuhan Sun ◽  
Xin Chen
Keyword(s):  
Cerebral Ischemia ◽  
Oxidative Damage ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Apoptosis Rate

Objective To assess the role of NOD-like receptor C5 (NLRC5; a major NLRC family protein that regulates immunity, inflammation and tissue fibrosis), in cerebral ischemia-reperfusion injury, characterized by inflammation and oxidative damage. Methods Blood NLRC5 levels were assessed in neonates with cerebral ischemia and in healthy controls. A stable PC12 cell line was established that overexpressed or knocked down NLRC5. Inflammatory responses, apoptosis rate and oxidative damage in PC12 cells under oxygen-glucose deprivation/reperfusion (OGD/R) conditions were evaluated using enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) and reactive oxygen species (ROS) assay. Results Blood NLRC5 levels were suppressed in neonates with cerebral ischemia. ELISAs showed that NLRC5 suppressed levels of tumour necrosis factor-α, interleukin (IL)-6, IL-1β, ROS and superoxide dismutase in OGD/R-treated PC12 cells. Furthermore, NLRC5 overexpression was associated with reduced apoptosis rate in PC12 cells treated by OGD/R. Overexpression of NLRC5 also inhibited levels of toll-like receptor (TLR)4, myeloid differentiation primary response protein MyD88 (MyD88) and phosphorylated nuclear factor kappa B-transcription factor p65 (NF-κB p-p65) in PC12 cells, and decreased nuclear levels of NF-κB p-p65. Conclusion NLRC5 alleviated inflammatory responses, oxidative damage and apoptosis in PC12 cells under OGD/R conditions by suppressing activation of the TLR4/MyD88/NF-κB pathway.

Glutathione supplementation and training increases myocardial resistance to ischemia-reperfusion in vivo

2001 ◽  
Vol 281 (2) ◽  
pp. H679-H688 ◽  
Author(s):  
P. R. Ramires ◽  
L. L. Ji
Keyword(s):  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Group Versus ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Lactate Dehydrogenase Release

The present study examined the effects of oral reduced glutathione (GSH) supplementation in conjunction with endurance training on contractile function, antioxidant defense, and oxidative damage in response to ischemia-reperfusion (I/R) in rat hearts. Female Sprague-Dawley rats (age 4 mo, n = 72) were randomly assigned to a treadmill-trained (T; 25 m/min, 15% grade, for 75 min/day, 5 days/wk, for 10 wk) or untrained (U) group. Each group was further divided into rats receiving 5 g GSH/kg diet during the final 17 days of training (GSH-S) and control (C) groups. One-half of each group of rats was subjected to I/R by surgical occlusion of the main coronary artery for 45 min, followed by 30-min reperfusion or sham operation. Left ventriclar (LV) peak systolic pressure (LVSP) and contractility (+dP/d t), measured with a catheter inserted into the LV via the carotid artery, decreased with I/R in all groups ( P< 0.05). However, LVSP with I/R in the T/GSH-S group was 9.5%, 17%, and 18% higher ( P < 0.05) than that in the U/GSH-S, T/C, and U/C groups, respectively. +dP/d t with I/R was 19%, 27%, and 29% ( P < 0.05) greater in the T/GSH-S group versus the T/C, U/GSH-S, and U/C groups, respectively. I/R decreased heart GSH content by 12–17% ( P < 0.05) and increased oxidized glutathione (GSSG) by 20–27% ( P < 0.05). T/GSH-S hearts showed 15% higher GSH ( P < 0.05) and a 32% higher GSH-to-GSSG ratio ( P < 0.05) than the U/C group at the end of I/R. Myocardial superoxide dismutase, GSH peroxidase, glutathione reductase, and γ-glutamyl transpeptidase activities were increased with treadmill training in both GSH-S and C rats. I/R induced myocardial lipid peroxidation and lactate dehydrogenase release were attenuated with T/GSH-S treatment. The present data indicate that training in conjunction with dietary GSH supplementation can increase myocardial GSH content and antioxidant defense capacity, thereby protecting the intact heart against oxidative damage and functional retardation caused by I/R.

scholarly journals Oxidative Damage in Clinical Ischemia/Reperfusion Injury: A Reappraisal

2013 ◽  
Vol 19 (6) ◽  
pp. 535-545 ◽  
Author(s):  
Dorottya K. de Vries ◽  
Kirsten A. Kortekaas ◽  
Dimitrios Tsikas ◽  
Leonie G.M. Wijermars ◽  
Cornelis J.F. van Noorden ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Effect of atorvastatin on oxidative damage and inflammation in experimental hindlimb ischemia–reperfusion model

2018 ◽  
Vol 16 ◽  
pp. 205873921881266
Author(s):  
Walter A Trujillo-Rangel ◽  
Araceli Castillo-Romero ◽  
Sylvia E Totsuka-Sutto ◽  
Simón Q Rodríguez-Lara ◽  
Teresa A García-Cobián ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cellular Damage ◽  
Healthy Controls ◽  
Transcript Levels ◽  
Loss And Damage ◽  
Ischemic Tissue ◽  
Tnf Α ◽  
Hematoxylin And Eosin Stain

Ischemia–reperfusion is defined as cellular damage after the reperfusion of ischemic tissue, and it is likely to occur in relation to various diseases and surgical procedures. The purpose of this study was to evaluate the capability of atorvastatin to prevent oxidative damage and modulate the release of proinflammatory cytokines in rat hindlimb during ischemia–reperfusion injury. The animals were divided into 4 groups (ischemia–reperfusion + vehicle, ischemia–reperfusion + atorvastatin, sham, and healthy controls) with 15 rats per group. The animals were exposed to ischemia for 6 h, followed by 24 h, 7 days, and 14 days of reperfusion. Atorvastatin was administered by gavage 14 days before ischemia–reperfusion induction. We then measured the serum concentrations and mRNA transcript levels of TNF-α, IL-1β, IL-6, IL-10, SOD2, and CAT. Hematoxylin and eosin stain were performed for histological analyses. Animals subjected to ischemia–reperfusion showed increased serum and transcript levels of TNF-α, IL-1β, IL-6, and IL-10 expressions with a concurrent increase in mRNA transcripts levels compared with sham and healthy controls. Groups treated with atorvastatin showed a significant CAT increase in the first 24 h, but CAT levels decreased at 7 and 14 days. SOD2 enzyme increased in serum without significant changes in mRNA expression. Histological analysis showed inflammatory infiltrate, microhemorrhages, and distortion of the tissue architecture in the first 7 days. At 14 days, the tissue showed loss and damage to myocytes. However, animals treated with atorvastatin showed few histological changes and a decrease in inflammatory cytokines. No significant changes in NO2, NO3, or 8-OHdG were observed. Atorvastatin showed a protective effect on the inflammation and tissue damage induced by ischemia–reperfusion in the hindlimb. The antioxidant effect of atorvastatin in the hindlimb is already unclear, and further research is needed to elucidate the molecular mechanism of this drug in the extremities.

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