Protective Effect of Superoxide Dismutase and Polyethylene Glycol-Linked Superoxide Dismutase Against Renal Warm Ischemia/Reperfusion Injury

Background: Renal ischaemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allografts, which is a complex pathophysiologic process involving hypoxia and free radical (FR) damage. The oil of Nigella sativa (NSO) has been subjected to considerable pharmacological investigations that have revealed its antioxidant activity in different conditions. But there is no previously reported study about its effect on ischaemia/reperfusion (I/R) injury of kidneys. The aim of this study was to investigate the possible effects of NSO in I/R-induced renal injury in rats. Methods: Thirty healthy male Wistar albino rats were randomly assigned to one of the following groups: control, sham, I/R, NSO+I/R, I/R+NSO and NSO. I/R, NSO+I/R and I/R+NSO rats were subjected to bilateral renal ischaemia followed by reperfusion and then all the rats were killed and kidney function tests, serum and tissue oxidants and antioxidants were determined and histopathological examinations were performed. Results: Pre-and post-treatment with NSO produced reduction in serum levels of blood urea nitrogen (BUN) and creatinine caused by I/R and significantly improved serum enzymatic activities of superoxide dismutase (SOD) and glutathion peroxidase (GSH-Px) and also tissue enzymatic activities of catalase (CAT), SOD and GSH-Px. NSO treatment resulted in lower total oxidant status (TOS) and higher total antioxidant capacity (TAC) levels and also significant reduction in serum and tissue malondialdehyde (MDA), nitric oxide (NO) and protein carbonyl content (PCC) that were increased by renal I/R injury. The kidneys of untreated ischaemic rats had a higher histopathological score, while treatment with NSO nearly preserved the normal morphology of the kidney. Conclusions: In view of previous observations and our data, with the potent FR scavenger and antioxidant propCorrespondence and offprint requests to: Nuket Bavbek, Dikmen Yildizi Sokak 10/8, DI . KMEN/ANKARA, 06460, Turkey. Tel: +90-0312-4838985/-4400606; Fax: +90-0312-2306080; E-mail: ntbavbek@yahoo.com erties, NSO seems to be a highly promising agent for protecting tissues from oxidative damage and preventing organ damage due to renal I/R.

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“…injury [3,29]. The decrease in renal CAT, SOD and GSH-Px activities is probably the result of the inactivation by ROS produced by I/R.…”

Section: Discussionmentioning

confidence: 99%

Nigella sativa protects against ischaemia/reperfusion injury in rat kidneys

Bayrak¹,

Bavbek²,

Karataş³

et al. 2008

Nephrology Dialysis Transplantation

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“…If free radical mediated lipid peroxidation remains uncontrolled, cell death will ultimately result. Experimentally various antioxidant agents such as superoxide dismutase, catalase, allopurinol, iloprost, and calcium channel blockers were used to prevent kidney from IR injury [1,3,11,12]. The role of reactive oxygen species in human kidney transplantation seems to correlate with results obtained in animal studies.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have suggested that in unilaterally nephrectomized rats, a 45-or 60-min ischemia period by clamping the renal pedicle results in ATN and a four-to fivefold increase in creatinine levels at the end of a 24-hour follow-up period [1,5,11,12]. In our experimental model, the plasma creatinine levels were elevated in the IC group as compared with the sham group at the end of the 75-min ischemia and 24-hour reperfusion periods (p !…”

Section: Discussionmentioning

confidence: 99%

Cytoprotective Effect of Trimetazidine on 75 min Warm Renal Ischemia-Reperfusion Injury in Rats

et al. 1998

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In this experimental study, we evaluated the effect of trimetazidine (TMZ) on renal ischemia-reperfusion (IR) injury in Sprague-Dawley rats. Renal IR was achieved by a 75-min clamping of the left renal pedicle and subsequent 24 h reperfusion, after right nephrectomy was performed. The rats were randomly divided into three groups: group 1 (sham operated: no IR injury), group 2 (ischemic control: saline treatment), and group 3 (3 mg/kg TMZ before ischemia). After 24 h of reperfusion, blood samples and renal tissue samples were taken to measure the levels of creatinine, tissue malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) activity. Histopathological changes were evaluated. In addition, the 7-day survival rates in each group were evaluated. We found significant increases in the levels of creatinine and tissue MDA, severe acute tubular necrosis, and a significant decrease in the activity of the GSH-Px in group 2. There were significant decreases in the levels of creatinine and tissue MDA, mild acute tubular necrosis, and a significant increase in activity of the GSH-Px in group 3 when compared with the control group (p <0.05). Statistically significant differences (p <0.05) in survival were noted between the ischemic control and sham-operated and TMZ groups. We have concluded that TMZ is able to protect the kidney from warm IR injury.

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“…Neutrophil activation at sites of injury results in a large production of •O 2 -, which in turn contributes to tissue damage seen post-reperfusion in several ischemic organs including: kidneys (76), stomach (114), skin (34), and heart (3). Cu/Zn-SOD prevents vasogenic brain edema after several kinds of injuries (60), suggesting that •O 2 -is an important factor for blood-brain barrier disruption (62).…”

Section: Ischemia/reperfusionmentioning

confidence: 99%

“…Important tissue damaging and pro-inflammatory roles attributed to •O 2 -include: endothelial cell damage and increased microvascular permeability (20,39,111), formation of chemotactic factors such as leukotriene B 4 (18,23), recruitment of neutrophils at sites of inflammation (10,94,95), lipid peroxidation and oxidation, and single-strand DNA damage (19). Superoxide anion radicals contribute to post-ischemic reperfusion tissue damage demonstrated in several organs (3,34,37,76,115 …”

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confidence: 99%

Superoxide dismutases: a physiopharmacological update

Valdivia

Perez-Alvarez²,

Aroca-Aguilar³

et al. 2009

J Physiol Biochem

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Reactive oxygen species (ROS) are known participants in several cellular processes. Superoxide anion radical, one example of ROS, forms as a result of normal cellular respiration and is usually cleared successfully by superoxide dismutase (SOD) and other radical scavengers. However, when superoxide exceeds the clearance capacity of SOD and other ROS scavengers, superoxide initiates a number of pathologic processes. This review examines pathologies involving superoxide, including: cancer, neurodegenerative diseases, ischemia/reperfusion injury, and inflammation. We will also explore the basic science principles of superoxide and SOD, including: SOD evolution, SOD mutations, biochemistry, physiology, and pathophysiology. In reviewing the basic science, clinical pathology, and therapeutic research, we hope to clearly demonstrate plausible pharmacologic targets of action. We have revised data about basic science, clinical pathology and therapeutic research in an effort to propose plausible pharmacological targets of action. The understanding of these aspects is critical in the accomplishment of a successful clinical intervention.

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Protective Effect of Superoxide Dismutase and Polyethylene Glycol-Linked Superoxide Dismutase Against Renal Warm Ischemia/Reperfusion Injury

Cited by 32 publications

References 8 publications

Nigella sativa protects against ischaemia/reperfusion injury in rat kidneys

Nigella sativa protects against ischaemia/reperfusion injury in rat kidneys

Cytoprotective Effect of Trimetazidine on 75 min Warm Renal Ischemia-Reperfusion Injury in Rats

Superoxide dismutases: a physiopharmacological update

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