Effects of boric acid on ovarian tissue damage caused by experimental ischemia/reperfusion

Author(s):  
Suat Çolak ◽  
Kubra Koc ◽  
Serkan Yıldırım ◽  
Fatime Geyikoğlu
2002 ◽  
Vol 46 (4) ◽  
pp. 345-349 ◽  
Author(s):  
N. SUCU ◽  
A. UNLU ◽  
L. TAMER ◽  
B. AYTACOĞLU ◽  
B. COSKUN ◽  
...  

Shock ◽  
2015 ◽  
Vol 43 (3) ◽  
pp. 268-275 ◽  
Author(s):  
Michael Kuncewitch ◽  
Weng-Lang Yang ◽  
Lana Corbo ◽  
Adam Khader ◽  
Jeffrey Nicastro ◽  
...  

Clinics ◽  
2013 ◽  
Vol 68 (7) ◽  
pp. 1034-1038 ◽  
Author(s):  
FJ Guzmán-de la Garza ◽  
JM Ibarra-Hernández ◽  
P Cordero-Pérez ◽  
P Villegas-Quintero ◽  
CI Villarreal-Ovalle ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Ramón Rodrigo ◽  
Matías Libuy ◽  
Felipe Feliú ◽  
Daniel Hasson

Acute myocardial infarction (AMI) is the leading cause of mortality worldwide. Major advances in the treatment of acute coronary syndromes and myocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty (PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing. The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could offer a novel therapeutic opportunity against this oxidative tissue damage.


1997 ◽  
Vol 273 (2) ◽  
pp. H989-H996 ◽  
Author(s):  
A. G. Harris ◽  
M. Steinbauer ◽  
R. Leiderer ◽  
K. Messmer

The purpose of this study was to examine the relationship of increased capillary network resistance due to leukocyte-capillary plugging and tissue edema through macromolecular leakage to tissue injury after ischemia-reperfusion (I/R). After a 3-h complete ischemia in the dorsal skinfold chamber of the awake Syrian hamster, the following parameters were measured: vessel diameter, macromolecular leakage, erythrocyte velocity, adherent leukocytes, rolling leukocytes, freely flowing leukocytes, functional capillary density (FCD), propidium iodide (PI)-positive cell nuclei, and increase in network flow resistance due to leukocyte-capillary plugging. These measurements were made under baseline conditions and after 0.5 and 2 h of reperfusion for I/R alone, I/R with phalloidin (PL) treatment (to block leakage), and I/R with both PL and cytochalasin D (CD) (to block both leakage and plugging). Neither treatment had an effect on the leukocyte adherence or rolling. PL treatment preserved the endothelial barrier, improved FCD, and reduced the amount of PI measured tissue damage. CD treatment eliminated the increase in network resistance due to leukocyte plugging but did not improve FCD or tissue damage. Thus, in this I/R model, macromolecular leakage plays a role in tissue injury, whereas leukocyte plugging does not appear to be an important mechanism.


PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e32260 ◽  
Author(s):  
Peter H. Lapchak ◽  
Antonis Ioannou ◽  
Lakshmi Kannan ◽  
Poonam Rani ◽  
Jurandir J. Dalle Lucca ◽  
...  

2011 ◽  
Vol 141 (1) ◽  
pp. 3-14 ◽  
Author(s):  
Antonis Ioannou ◽  
Jurandir Dalle Lucca ◽  
George C. Tsokos

Sign in / Sign up

Export Citation Format

Share Document