The Protective Effects of Ascorbic Acid against Renal Ischemia-Reperfusion Injury in Male Rats

Korkmaz, Ali; Kolankaya, Diirdane

doi:10.1080/08860220802546271

Cited by 86 publications

(69 citation statements)

References 32 publications

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“…2,[25][26][27] In this study, pretreatment with fenofibrate alone and in combination with telmisartan for two consecutive weeks effectively protected against Table 2. Renal MDA, GSH, NO, and MPO levels of all experimental groups.…”

Section: Discussionmentioning

confidence: 99%

Role of fenofibrate alone and in combination with telmisartan on renal ischemia/reperfusion injury

et al. 2010

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It was demonstrated that fenofibrate and telmisartan exerted renoprotective effects in ischemia/reperfusion (I/R) injury. Because the combination of fenofibrate and telmisartan synergistically enhanced peroxisome proliferator-activated receptor (PPAR) activation, we hypothesized that the combination of both drugs may exert prolonged beneficial effects in renal I/R injury than fenofibrate alone. Forty-eight male Wistar albino rats were divided into eight groups. Hyperlipidemia was induced by cholesterol feeding for 4 weeks. At the end of the fourth week, renal I/R injury was performed by occlusion of both renal vascular pedicles for 60 minutes, followed by 24 hours of reperfusion. In the treatment group, fenofibrate alone and in combination with telmisartan was administered 2 weeks prior to renal ischemia. At the end of the experiment, blood and kidneys were isolated for biochemical and histological analysis. I/R in hyperlipidemic rat shows significantly increased lipid peroxidation, nitric oxide, and myeloperoxidase activity, and depletion of antioxidant enzyme compared with control rats, and that was significantly restored after fenofibrate and telmisartan treatment. Also, significant increases in serum homocysteine level were detected following I/R. Fenofibrate treatment further elevated homocysteine level, which was reduced by telmisartan in combination with fenofibrate. The most significant histological damage was found in the hyperlipidemic rat subjected to renal I/R, which was reduced significantly with combination therapy. The results of this study concluded that fenofibrate alone and in combination with telmisartan significantly ameliorated renal I/R injury. The additive beneficial effect of telmisartan is predicted to reduce homocysteine-induced oxidative stress through reduced nitric oxide production during I/R.

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Section: Discussionmentioning

confidence: 99%

Role of fenofibrate alone and in combination with telmisartan on renal ischemia/reperfusion injury

et al. 2010

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“…38 We have previously shown that uninephrectomy did not alter the renal parameters (serum creatinine, blood urea nitrogen). 39,40 Furthermore, we showed that the renal I/R treatment (45 min of ischemia followed by 3 h of reperfusion) impaired glomerular function by increasing serum blood urea nitrogen and creatinine levels in rats. 39,40 Therefore, the experimental model of renal I/R that we used in the present study is suitable to demonstrate the potential iNOS inhibiting role of rutin in I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Korkmaz

Kolankaya

2013

Can J Surg

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Background: Nitric oxide (NO) seems to play an important role during renal ischemia/reperfusion (I/R) injury. We investigated whether rutin inhibits inducible nitric oxide synthase (iNOS) and reduces 3-nitrotyrosine (3-NT) formation in the kidneys of rats during I/R. Methods:Wistar albino rats were nephrectomized unilaterally and, 2 weeks later, subjected to 45 minutes of left renal pedicle occlusion followed by 3 hours of reperfusion. We intraperitoneally administered L-N6-(1-iminoethyl)lysine (L-NIL; 3 mg/kg) for 30 minutes or rutin (1 g/kg) for 60 minutes before I/R. After reperfusion, kidney samples were taken for immunohistochemical analysis of iNOS and 3-NT. We measured plasma nitrite/nitrate and cyclic guanosine monophosphate (cGMP) to evaluate NO levels.Results: Ischemia/reperfusion caused plasma cGMP to increase significantly. Similarly, plasma nitrite/nitrate was elevated in the I/R group compared with the control group. Histochemical staining was positive for iNOS and 3-NT in the I/R group. Pretreatment with L-NIL or rutin significantly mitigated the elevation of plasma cGMP and nitrite/nitrate. These changes in biochemical parameters were also associated with changes in immunohistochemical appearance. Pretreatment with L-NIL or rutin significantly decreased the incidence and severity of iNOS and 3-NT formation in the kidney tissues. Conclusion:Our findings suggest that high activity of iNOS causes renal I/R injury, and that rutin exerts protective effects, probably by inhibiting iNOS.Contexte : L'oxyde nitrique (NO) semble jouer un rôle important durant la lésion d'ischémie/reperfusion (I/R) rénale. Nous avons vérifié si la rutine inhibe l'oxyde nitrique synthase inductible (iNOS) et réduit la formation de 3-nitrotyrosine (3-NT) dans les reins de rats durant l'I/R. Méthodes :Des rats albinos Wistar ont subi une néphrectomie unilatérale avant d'être soumis 2 semaines plus tard à une occlusion du pédicule rénal gauche d'une durée de 45 minutes, suivie de 3 heures de reperfusion. Nous avons administré de la L-N6-(1-iminoéthyl)lysine (L-NIL; 3 mg/kg) par voie intrapéritonéale pendant 30 minutes ou de la rutine (1 g/kg) pendant 60 minutes avant l'I/R. Après la reperfusion, des échantillons de tissu rénal ont été prélevés pour analyse immunohistochi mique de l'iNOS et de la 3-NT. Nous avons mesuré les taux plasmatiques de nitrite/nitrate et de guanosine monophosphate cyclique (cGMP) pour évaluer les taux de NO.

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“…Studies have shown that vitamin C has antioxidant and protective properties against oxidative damage formed by free radicals [14,24]. On the contrary, it has been shown that supplementation of ascorbic acid into the culture medium induced apoptotic cell death by displaying prooxidant action [37].…”

Section: Introductionmentioning

confidence: 99%

Antioxidant defense system parameters in isolated fish hepatocytes exposed to bisphenol A — Effect of vitamin C

Kaya¹,

Kaptaner²

2016

Acta Biologica Hungarica

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In this study, isolated hepatocytes of pearl mullet (Alburnus tarichi) were exposed to bisphenol A (BPA) at concentrations of 25, 50, 100, and 200 µM for 24 h. Moreover, an in vitro antioxidant concentration of vitamin C (50 µM) was administrated to the culture medium along with the BPA exposures. Next, the antioxidant defense system parameters were analyzed. According to the results, the highest concentration of BPA (200 µM) proved to be severely toxic for the cells. The increased activities of superoxide dismutase (SOD) and glutathione-S-transferase (GST), the fluctuated activities of glutathione peroxidase (GPx), and the decreased content of reduced glutathione (GSH) were compared to the control group after the BPA exposures. Vitamin C co-administration was found to cause further increases in the SOD, GPx, and GST activities in some of the experimental groups and vitamin C could not restore the GSH content. Malondialdehyde (MDA) levels were observed to be unaffected in all exposure groups. These results show that BPA causes alterations in the antioxidant defenses of the isolated fish hepatocytes. In addition, vitamin C co-administration along with BPA was found to be non-protective against BPA-induced oxidative stress, consequently, aggravated a negative BPA impact.

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The Protective Effects of Ascorbic Acid against Renal Ischemia-Reperfusion Injury in Male Rats

Cited by 86 publications

References 32 publications

Role of fenofibrate alone and in combination with telmisartan on renal ischemia/reperfusion injury

Role of fenofibrate alone and in combination with telmisartan on renal ischemia/reperfusion injury

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Antioxidant defense system parameters in isolated fish hepatocytes exposed to bisphenol A — Effect of vitamin C

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