Comparison of the Efficacy of Melatonin and 1400W on Renal Ischemia/Reperfusion Injury: A Role for Inhibiting iNOS

Ersöz, Nail; Güven, Ahmet; Çaycı, Tuncer; Uysal, Bülent; Türk, Emin; Öztaş, Emin; Akgül, Emin Özgür; Korkmaz, Ahmet; Çetiner, Sadettin

doi:10.3109/08860220903085989

Cited by 35 publications

(39 citation statements)

References 39 publications

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“…It is well known that MDA serves as a reliable marker of free oxygen radical mediated lipid peroxidation. 10,28 So, our results clearly showed that SWT procedure increases free oxygen radical causing renal cellular injury, especially that caused by peroxidation of cellular membrane lipids and oxidation of cellular proteins. However, we measured SOD and GSH-Px enzyme activities to evaluate renal oxidative stress level.…”

Section: Discussionmentioning

confidence: 58%

“…6,29,31 Supporting these observations have come from various in vivo studies which shown that NO biosynthesis and its action are closely related to the pathogenesis of renal ischemia reperfusion injury. 10,33 The role of NO in the development of renal ischemia reperfusion injury has been also confirmed in several investigations in which administration of iNOS inhibitors protected the kidney against ischemia reperfusion injury. 31 In addition, it was shown that the kidneys of iNOS knockout mice are resistant to hypoxic injury, whereas eNOS knockout or neuronal NOS knockout mice were not.…”

mentioning

confidence: 85%

“…Intensified expression of iNOS has been detected virtually in all cell types tested including macrophages, fibroblasts, chondrocytes, osteoclasts, and epithelial cells and results in the production of large amounts of NO in animals and patients with inflammatory diseases. 10,11 It has been demonstrated that SWT causes rapid enhancement of endothelial nitric oxide synthase (eNOS) activity in SWT-treated cells resulting in increased NO levels. 3 Moreover, it was reported that shock waves stimulate the NO-cyclic 3 0 -5 0 -guanosine monophosphate signaling pathway and increase mean plasma nitrite levels in patient with renal stones.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury

Fırat¹,

Malkoç

Demirer³

et al. 2014

Renal Failure

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Objectives: Shock wave lithotripsy treatment (SWT) is not completely free from side effects; one of the accused mechanisms for renal injury during SWT is oxygen-and nitrogen-derived free radical productions. Therefore, we aimed to evaluate the effect of inhibition of nitric oxide (NO) production by N-[3(aminomethyl) benzyl) acetamidine] (1400W), highly selective inducible nitric oxide synthase (iNOS) inhibitor, at SWT-induced kidney damage. Materials and methods: Twenty-four rats those underwent right nephrectomy procedure were divided equally into three groups as control, SWT, and SWT + 1400W. 1400W was administered at a dose of 10 mg/kg at 2 h prior to SWT procedure and at the beginning of SWT procedure via intraperitoneal route and continued daily for consecutive 3 days. At the end of the fourth day, animals were killed via decapitation and trunk blood and the left kidneys were taken for biochemical and histopathologic evaluation. Results: SWT caused renal tubular damage and increased lipid peroxidation and antioxidant enzyme activities and SWT also significantly increased nitro-oxidative products. Inhibition of iNOS via administration of 1400W ameliorated renal injury and decreased tissue lipid peroxidation (malondialdehyde), superoxide dismutase, glutathione peroxidase and nitrite/nitrate levels (NO x ). In addition, it was seen that histolopathological changes were attenuated in the SWT + 1400W group when compared to SWT group. Conclusion: SWT-induced renal injury might be due to excessive production of oxygen free radicals and NO production. Inhibition of iNOS attenuates renal injury following SWT treatment. It can be concluded that iNOS inhibitors or peroxynitrite scavengers might be used to protect the kidneys against SWT-induced morphological and functional injuries.

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Section: Discussionmentioning

confidence: 58%

mentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

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Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury

Fırat¹,

Malkoç

Demirer³

et al. 2014

Renal Failure

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“…Nitrate/nitrite (NO x ) levels, end products of NO degradation, were measured using the method described by Miranda et al, as we described in our previous studies. 4,5,11 …”

Section: Biochemical Analysismentioning

confidence: 99%

“…2,3,9,10 It is well documented in several studies that scavenging of ROS from kidney would protect it from IRI, while RNS might continue to cause cellular damage. 4,11 Therefore, scavenging of both ROS and RNS in IRI may be more beneficial.…”

Section: Introductionmentioning

confidence: 99%

Beneficial Effects ofN-Acetylcysteine and Ebselen on Renal Ischemia/Reperfusion Injury

et al. 2011

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Introduction: It has been demonstrated that peroxynitrite accompanies acute renal ischemia and contributes to the pathophysiology of renal damage. Therefore, we aimed to investigate the roles of N-acetylcysteine (NAC), a well-known powerful antioxidant, and ebselen (E), a scavenger of peroxynitrite, on renal injury induced by renal ischemia/reperfusion injury (IRI) of rat kidney. Materials and methods: Forty male Sprague-Dawley rats were divided into five groups: sham, renal IRI, renal IRI+NAC, renal IRI+E, and renal IRI+NAC+E. IR injury was induced by 60 min of bilateral renal ischemia followed by 6 h of reperfusion. After reperfusion, kidneys and blood samples were obtained for histopathological and biochemical evaluations. Results: Renal IR resulted in increased malondialdehyde and nitrite/nitrate levels suggesting increased lipid peroxidation and peroxynitrite production and decreased superoxide dismutase and glutathione peroxidase activities. Both NAC and E alone significantly decreased malondialdehyde and nitrite/nitrate levels and increased superoxide dismutase and glutathione peroxidase activities. Additionally in the renal IRI+NAC+E group, all biochemical results were quite close to those of sham group. Histopathologically, the kidney injury in rats treated with combination of NAC and E was found significantly less than the other groups. Conclusions: Both NAC and E are able to ameliorate IRI of the kidney by decreasing oxidative and nitrosative stresses and increasing free radical scavenger properties. Additionally, combination of NAC and E prevents kidney damage more than when each drug is used alone, suggesting that scavenging peroxynitrite nearby antioxidant activity is important in preventing renal IRI.

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A preclinical study on the protective effect of melatonin against methotrexate-induced small intestinal damage: effect mediated by attenuation of nitrosative stress, protein tyrosine nitration, and PARP activation

Kolli

Kanakasabapathy

Faith

et al. 2013

Cancer Chemother Pharmacol

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Comparison of the Efficacy of Melatonin and 1400W on Renal Ischemia/Reperfusion Injury: A Role for Inhibiting iNOS

Cited by 35 publications

References 39 publications

Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury

Inhibition of inducible nitric oxide synthase prevents shock wave therapy induced renal injury

Beneficial Effects ofN-Acetylcysteine and Ebselen on Renal Ischemia/Reperfusion Injury

A preclinical study on the protective effect of melatonin against methotrexate-induced small intestinal damage: effect mediated by attenuation of nitrosative stress, protein tyrosine nitration, and PARP activation

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