scholarly journals Hydroxyl radical induced structural changes of collagen

2007 ◽  
Vol 21 (2) ◽  
pp. 91-103 ◽  
Author(s):  
Helan Xiao ◽  
Guoping Cai ◽  
Mingyao Liu
Keyword(s):  
Free Radical ◽  
Hydroxyl Radicals ◽  
Structural Changes ◽  
Type I Collagen ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Type I ◽  
Dependent Manner ◽  
First Time

Extracellular matrix (ECM) plays an important role in cell differentiation, growth, migration and apoptosis. Collagen is the most abundant protein familyin vivo, but its function has still not been clearly defined yet. Reactive oxygen species (ROS) have a central role in oxidative cell stress. Electron spin resonance (ESR) spectroscopy indicates that type I collagen could uniquely scavenge hydroxyl radicals in dose- and time-dependent manner; whereas BSA and gelatin (a denatured collagen) have no such an effect. However, the mechanism by which type I collagen scavenges hydroxyl radicals is different from that of GSH, a well-known free radical scavenger. Using a new method, two-dimensional FTIR correlation analysis, for the first time, we show that the order of functional group changes of type I collagen in this process is amide I earlier than amide II than amide III than –CH– thanν(C=O). The results indicates that the structure of the main chain of collagen changed first, followed by more residue groupν(C=O) exposed to hydroxyl radicals. The reaction with the carbonyl group in collagen causes the hydroxyl free radicals to be scavenged. Therefore, ECM can effectively scavenge ROS under normal physiological conditions. When the proteins of ECM were denatured in the same way as gelatin, they lost their function as a free radical scavenger. All of these results provide new insight into therapy or prevention of oxidative stress, apoptosis and ageing.

Alterations in free radical scavenger system profile of type I diabetic rat brain

1998 ◽  
Vol 35 (1-3) ◽  
pp. 187-202 ◽  
Author(s):  
Sanjeev Kumar Bhardwaj ◽  
Poonam Sharma ◽  
Gurcharan Kaur
Keyword(s):  
Free Radical ◽  
Rat Brain ◽  
Free Radical Scavenger ◽  
Diabetic Rat ◽  
Radical Scavenger ◽  
Type I

scholarly journals Phenyl N -tert-butylnitrone, a Free Radical Scavenger, Reduces Mechanical Allodynia in Chemotherapy-induced Neuropathic Pain in Rats

2010 ◽  
Vol 112 (2) ◽  
pp. 432-439 ◽  
Author(s):  
Hee Kee Kim ◽  
Yan Ping Zhang ◽  
Young Seob Gwak ◽  
Salahadin Abdi
Keyword(s):  
Neuropathic Pain ◽  
Free Radical ◽  
Mechanical Allodynia ◽  
Intraperitoneal Administration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Dose Dependent

Background Paclitaxel is a widely used chemotherapeutic drug for breast and ovarian cancer. Unfortunately, it induces neuropathic pain, which is a dose-limiting side effect. Free radicals have been implicated in many neurodegenerative diseases. The current study tests the hypothesis that a free radical scavenger plays an important role in reducing chemotherapy-induced neuropathic pain. Methods Neuropathic pain was induced by intraperitoneal injection of paclitaxel (2 mg/kg) on four alternate days (days 0, 2, 4, and 6) in male Sprague-Dawley rats. Phenyl N-tert-butylnitrone (PBN), a free radical scavenger, was administered intraperitoneally as a single dose or multiple doses before or after injury. Mechanical allodynia was measured by using von Frey filaments. Results The administration of paclitaxel induced mechanical allodynia, which began to manifest on days 7-10, peaked within 2 weeks, and plateaued for at least 2 months after the first paclitaxel injection. A single injection or multiple intraperitoneal injections of PBN ameliorated paclitaxel-induced pain behaviors in a dose-dependent manner. Further, multiple administrations of PBN starting on day 7 through day 15 after the first injection of paclitaxel completely prevented the development of mechanical allodynia. However, an intraperitoneal administration of pbn for 8 days starting with the first paclitaxel injection did not prevent the development of pain behavior. Conclusions This study clearly shows that PBN alleviated mechanical allodynia induced by paclitaxel in rats. Furthermore, our data show that PBN given on days 7 through 15 after the first paclitaxel injection prevented the development of chemotherapy-induced neuropathic pain. This clearly has a clinical implication.

scholarly journals SENP3 regulates high glucose-induced endothelial dysfunction via ROS dependent signaling

2020 ◽  
Vol 17 (6) ◽  
pp. 147916412097089
Author(s):  
Fuheng Chen ◽  
Dongdong Ma ◽  
Aizhong Li
Keyword(s):  
Endothelial Dysfunction ◽  
High Glucose ◽  
Type I Diabetes ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Type I ◽  
Dependent Manner ◽  
Glucose Levels ◽  
And Migration

Background: The current study aimed to explore the role of SENP3 in endothelial cell dysfunction in a high-glucose setting. Methods: The gene and protein expressions of SENP3 in high-glucose cultured HAECs were examined using quantitative PCR and western blotting. The effects of SENP3 on HAEC viability, apoptosis, migration, and endothelial–monocyte adhesion were evaluated in vitro by knockdown. Moreover, a mouse streptozotocin-induced type I diabetes model was established for SENP3 expression assessment. In addition, the effects of SENP3 on ROS-related signaling pathways were investigated in high-glucose cultured HAECs. Results: Significantly increased levels of SENP3 mRNA and protein were found in high-glucose cultured HAECs in a time-dependent manner. SENP3 knockdown reversed high glucose-induced HAEC viability, apoptosis, and migration reduction. SENP3 knockdown attenuated the high glucose-induced intercellular adhesion of THP-1 monocytic cells and HAECs via downregulation of ICAM-1 and VCAM-1 expression. Increased levels of SENP3, ICAM-1, and VCAM-1 expression were observed in the aorta tissue of mice with type I diabetes. Downregulation of SENP3 expression was observed in HAECs cultured with high glucose levels using the free radical scavenger N-acetyl-L-cysteine or NOX4 siRNA. Conclusions: SENP3 was involved in high glucose-induced endothelial dysfunction, and ROS-dependent signaling served as the mechanism.

Ceria-Zirconia Antioxidant Nanoparticles Attenuate Hypoxia-Induced Acute Kidney Injury by Restoring Autophagy Flux and Alleviating Mitochondrial Damage

2020 ◽  
Vol 16 (7) ◽  
pp. 1144-1159
Author(s):  
Sang-Eun Hong ◽  
Jong Hun An ◽  
Seong-Lan Yu ◽  
Jaeku Kang ◽  
Chang Gyo Park ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Free Radical ◽  
Antioxidant Activities ◽  
Kidney Injury ◽  
Mitochondrial Damage ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Autophagy Flux ◽  
Novel Approach

Oxidative stress is one of the principal causes of hypoxia-induced kidney injury. The ceria nanoparticle (CNP) is known to exhibit free radical scavenger and catalytic activities. When zirconia is attached to CNPs (CZNPs), the ceria atom tends to remain in a Ce3+ form and its efficacy as a free radical scavenger thus increases. We determined the effectiveness of CNP and CZNP antioxidant activities against hypoxia-induced acute kidney injury (AKI) and observed that these nanoparticles suppress the apoptosis of hypoxic HK-2 cells by restoring autophagy flux and alleviating mitochondrial damage. In vivo experiments revealed that CZNPs effectively attenuate hypoxia-induced AKI by preserving renal structures and glomerulus function. These nanoparticles can successfully diffuse into HK-2 cells and effectively counteract reactive oxygen species (ROS) to block hypoxia-induced AKI. This suggests that these particles represent a novel approach to controlling this condition.

A Novel Free Radical Scavenger, Edarabone, Protects Against Cisplatin-Induced Acute Renal Damage in Vitro and in Vivo

2003 ◽  
Vol 305 (3) ◽  
pp. 1183-1190 ◽  
Author(s):  
Minoru Satoh ◽  
Naoki Kashihara ◽  
Sohachi Fujimoto ◽  
Hideyuki Horike ◽  
Takehiko Tokura ◽  
...  
Keyword(s):  
Free Radical ◽  
Renal Damage ◽  
Free Radical Scavenger ◽  
Radical Scavenger

MCI-186 (edaravone), a novel free radical scavenger, protects against acute autoimmune myocarditis in rats

2005 ◽  
Vol 289 (6) ◽  
pp. H2514-H2518 ◽  
Author(s):  
Masaomi Nimata ◽  
Taka-aki Okabe ◽  
Miki Hattori ◽  
Zuyi Yuan ◽  
Keisuke Shioji ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Hydroxyl Radicals ◽  
Radical Scavenging ◽  
Weight Ratio ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Cytotoxic Activities ◽  
Thiobarbituric Acid Reactive Substance ◽  
Autoimmune Myocarditis

In this study, we tested the hypothesis that MCI-186 (3-methyl-1-phenyl-2-pyrazolin-5-one; edaravone), a novel free radical scavenger, protects against acute experimental autoimmune myocarditis (EAM) in rats by the radical scavenging action associated with the suppression of cytotoxic myocardial injury. Recent evidence suggests that oxidative stress may play a role in myocarditis. We administered MCI-186 intraperitoneally at 1, 3, and 10 mg·kg−1·day−1 to rats with EAM for 3 wk. The results were compared with untreated rats with EAM. MCI-186 treatment did not affect hemodynamics. MCI-186 treatment (3 and 10 mg·kg−1·day−1) reduced the severity of myocarditis as assessed by comparing the heart-to-body weight ratio and pathological scores. Myocardial interleukin-1β (IL-1β)-positive cells and myocardial oxidative stress overload with DNA damage in rats with EAM given MCI-186 treatment were significantly less compared with those of the untreated rats with EAM. In addition, MCI-186 treatment decreased not only the myocardial protein carbonyl contents but also the myocardial thiobarbituric acid reactive substance products in rats with EAM. The formation of hydroxyl radicals in MCI-186-treated heart homogenates was decreased compared with untreated heart homogenates. Furthermore, cytotoxic activities of lymphocytes of rats with EAM treated with MCI-186 were significantly lower compared with those of the untreated rats with EAM. Hydroxyl radicals may be involved in the development of myocarditis. MCI-186 protects against acute EAM in rats associated with scavenging hydroxyl free radicals, resulting in the suppression of autoimmune-mediated myocardial damage associated with reduced oxidative stress state.

A novel free radical scavenger rescues retinal cells in vivo

2011 ◽  
Vol 93 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Carolyn O’Driscoll ◽  
Francesca Doonan ◽  
Nuria Sanvicens ◽  
Angel Messeguer ◽  
Thomas G. Cotter
Keyword(s):  
Free Radical ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Retinal Cells
Sign in / Sign up

Export Citation Format

Share Document