Comparative modulating effects of captopril, diltiazem, dietary calcium and pyridoxal-5′-phosphate on gentamicin-induced nephrotoxicity in the rat

Ali, Badreldin H.; Bashir, A.A.

doi:10.1016/0306-3623(93)90381-7

Cited by 13 publications

(8 citation statements)

References 16 publications

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“…The fodipir moiety binds to the pyridoxal 5′ phosphate receptor on hepatocytes and ensures a high intrahepatic concentration of mangafodipir in the liver. In addition to the known capability of fodipir to increase GSH levels under a variety of oxidative conditions [24]–[26], we have shown that mangafodipir displays pleiotropic antioxidant properties. Indeed, this molecule is endowed with SOD-, catalase-, and glutathione reductase-like activities that allow both detoxification of mitochondrial ROS and regeneration of the GSH pool [27].…”

Section: Introductionmentioning

confidence: 86%

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

et al. 2011

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Introduction and AimMangafodipir is a contrast agent used in magnetic resonance imaging that concentrates in the liver and displays pleiotropic antioxidant properties. Since reactive oxygen species are involved in ischemia-reperfusion damages, we hypothesized that the use of mangafodipir could prevent liver lesions in a mouse model of hepatic ischemia reperfusion injury. Mangafodipir (MnDPDP) was compared to ischemic preconditioning and intermittent inflow occlusion for the prevention of hepatic ischemia-reperfusion injury in the mouse.MethodsMice were subjected to 70% hepatic ischemia (continuous ischemia) for 90 min. Thirty minutes before the ischemic period, either mangafodipir (10 mg/kg) or saline was injected intraperitoneally. Those experimental groups were compared with one group of mice preconditioned by 10 minutes' ischemia followed by 15 minutes' reperfusion, and one group with intermittent inflow occlusion. Hepatic ischemia-reperfusion injury was evaluated by measurement of serum levels of aspartate aminotransferase (ASAT) activity, histologic analysis of the livers, and determination of hepatocyte apoptosis (cytochrome c release, caspase 3 activity). The effect of mangafodipir on the survival rate of mice was studied in a model of total hepatic ischemia.ResultsMangafodipir prevented experimental hepatic ischemia-reperfusion injuries in the mouse as indicated by a reduction in serum ASAT activity (P<0.01), in liver tissue damages, in markers of apoptosis (P<0.01), and by higher rates of survival in treated than in untreated animals (P<0.001). The level of protection by mangafodipir was similar to that observed following intermittent inflow occlusion and higher than after ischemic preconditioning.ConclusionsMangafodipir is a potential new preventive treatment for hepatic ischemia-reperfusion injury.

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Section: Introductionmentioning

confidence: 86%

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

et al. 2011

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“…Captopril has been found to, potentiated GM-induced nephrotoxicity by increasing serum creatinine and urea concentrations and inducing severe necrosis of proximal convoluted tubule (PCT) [13]. However, captopril has been demonstrated to have a beneficial role in protecting GM-induced nephropathy [14,15]. The present study was designed to conclude whether ENAL would alter the pathophysiological changes induced in the kidney by GM.…”

Section: Introductionmentioning

confidence: 99%

The Nephrotoxicity of Concurrent Use of Enalapril and Gentamicin in Rats

Al-Ani

Algantri²,

Nafie

et al. 2018

Asian J Pharm Clin Res

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Objective: The present study was aimed to assess the concurrent administration of Enalapril (ENAL) and Gentamicin (GM) in the kidney of rats.Methods: Sixty male Sprague Dawley rats were divided into 4 main groups (n=15) according to the administered dose. Each main group was further subdivided into three subgroups according to the day of sacrificing (n=5). Group (C) was administered daily with normal saline as control, Group (E) was treated with oral ENAL (2 mg/kg/day), Group (G) was treated with GM (75 mg/kg/day), and Group (EG) was treated ENAL (2 mg/kg/day) and GM (75 mg/kg/day). The handling of the experiment persisted daily for 15 days, and the investigational examination carried out on days 5, 10, and 15.Results: The result showed that GM nephrotoxicity augmented with the period of the experimental study, there was rising in the levels of serum creatinine and blood urea nitrogen on the 10th day and persisted in rising significantly during the period on the 15th day of the experiment. Administration of ENAL showed no significant alteration from those of controls. While the concurrent administration of ENAL and GM showed that ENAL gradually increased GM nephrotoxicity, these physiological retrogressions were accompanied with intensive renal histopathological deteriorations.Conclusion: The present study has revealed that the concurrent administration of ENAL enormously aggravated the functional and histological nephrotoxicity of GM in rats.

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“…Group V was known as captapril group which received captopril as 10mg/kg/day per oral by oral gavage (Capoten, 25mg, Pharmadex, American) for 15 days [6]. 6.…”

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confidence: 99%

“…Group VI was known as Acute Renal Failure (ARF) and captapril group which receive injection of gentamicin 100mg/kg/day and oral captopril of 10mg/kg/day for 15 days [6]. At the end of the study all experimental animals were weighted.…”

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confidence: 99%

Renoprotective effect of inhibiting renin-angiotensin-aldosterone system (RAAS) by captopril versus losartan on drug-induced acute kidney injury (AKI)

Zafar¹

2018

PAB

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Renoprotective effect of inhibiting renin-angiotensin-aldosterone system (RAAS) by captopril versus losartan on drug-induced acute kidney injury (AKI). AbstractAcute kidney injury (AKI) is a common health problem especially the drug induced AKI is a side or toxic effect during treatment of different medical disorders. The present study was aimed to investigate the renoprotective effect of inhibiting renin-angiotensin-aldosterone system (RAAS) by captopril versus losartan on drug induced acute kidney injury (AKI). In this study sixty (60) male albino rats divided into six groups (10 rats/group); control, AKI. AKI+captopril, AKI+losartan, captopril and losartan have been used. GFR (glomerular filteration rate) and SBP (systolic blood pressure) have been measured. For measurement of MCP-1 (monocyte chemoattractant protein-1), urea, NGAL (Neutrophil gelatinaseassociated lipocalin, ICAM-1 (intercellular adhesion molecule -1), cystatin-C and creatinine serum samples were collected. Kidney tissues for measurement of tissue of KIM-1 (Kidney injury molecule-1), MDA (malondialdehyde) and renal expression of megalin were removed. Both losartan and captopril attenuated drug induced acute kidney injury (AKI) as revealed from the measured tissue parameters and serum. As compared to losartan, captopril was found to be superior on normalizing KIM-1, megalin and ICAM-1 while as compared to captopril, losartan improved more GFR. In AKI, groups treated with captopril and groups treated with losartan showed no significant difference in such type of measured parameters. Both are used for acute kidney injury and losartan slow the rate of progression of the experimental renal disease as compared to captopril in future case.

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Comparative modulating effects of captopril, diltiazem, dietary calcium and pyridoxal-5′-phosphate on gentamicin-induced nephrotoxicity in the rat

Cited by 13 publications

References 16 publications

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

Mangafodipir Protects against Hepatic Ischemia-Reperfusion Injury in Mice

The Nephrotoxicity of Concurrent Use of Enalapril and Gentamicin in Rats

Renoprotective effect of inhibiting renin-angiotensin-aldosterone system (RAAS) by captopril versus losartan on drug-induced acute kidney injury (AKI)

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