Protective effect of oral l-arginine administration on gentamicin-induced renal failure in rats

Can, Cenk; Şen, Sait; Boztok, N; Tuglular, I.

doi:10.1016/s0014-2999(00)00025-x

Cited by 38 publications

(34 citation statements)

References 19 publications

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“…This precursor, furthermore, prevented the appearance of the histopathological findings and also the increase in plasma levels of BUN and creatinine. These findings give support to the previous study by Can et al [12], who also reported that L -NAME, an NO synthase inhibitor [21], reversed the protective effect of L -arginine. NO has been shown to be basally released from isolated perfused kidney and to regulate both renal dynamic and tubular functions [10].…”

Section: Discussionsupporting

confidence: 92%

“…The prevention of nephrotoxicity therefore has a crucial clinical value. It has been reported that inhibition of NO synthesis is an important factor in renal failure [11] and that L -arginine supplementation has a protective role in gentamicin-induced renal failure [12], suggesting a possible pathophysiological role for endogenous NO levels in renal disease. In the present study, L-arginine, a precursor for the synthesis of NO [20,] normalized the decreased vasorelaxant responses induced by Ach, SNP, and PIN in isolated perfused kidney from gentamicin-treated rats.…”

Section: Discussionmentioning

confidence: 99%

“…Tubular necrosis was graded (I–III) as follows: grade I (mild): areas of subcapsular tubular necrosis in small foci; grade II (moderate): tubular necrosis at different foci throughout the cortex, and grade III (severe): extensive and marked tubular necrosis throughout the cortex. Tubular regeneration, presence of tubulointerstitial mononuclear cell infiltration was graded similarly [12]. …”

Section: Methodsmentioning

confidence: 99%

“…It has been reported that NO plays an important role not only in the regulation of renal hemodynamics but also renal tubular function [10] and that impairment in its synthetic pathway is involved in the renal failure [11]. A previous study demonstrated that gentamicin, an aminoglycoside antibiotic, decreased the glomerular filtration, and this reduction was reversed by co-administration of L -arginine [12]. Furthermore, trapidil, an antiplatelet and vasodilator agent which increased serum NO metabolites, attenuated gentamicin-induced renal failure [13].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of <i>L</i>-Arginine Intake on the Impaired Renal Vascular Responses in the Gentamicin-Treated Rats

Seçilmiş¹,

Karataş²,

Yorulmaz³

et al. 2005

Nephron Physiol

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The purpose of this study was to investigate the effect of gentamicin (100 mg/kg/day, i.p.) treatment on endothelium-dependent and -independent vasodilation in isolated perfused rat kidney, and the effect of amino acid L-arginine (in the drinking water, 2.25 g/l) on renal dysfunction induced by gentamicin. When gentamicin-treated groups were compared with the control group, it was observed that BUN and creatinine levels increased significantly. Also, the relaxant responses induced by acetylcholine, sodium nitroprusside and pinacidil decreased. Histopathological examination indicated acute tubular necrosis in this group. In animals treated with gentamicin together with L-arginine, there was a significant amelioration in the BUN and creatinine levels. The vasodilator responses were similar to those of the control group. Histopathological examination indicated only hydropic degeneration in tubular epithelium of kidney. Co-administration of L-N^G-nitroarginine methyl ester (L-NAME) (112.5 mg/l), an inhibitor of nitric oxide synthase, and L-arginine to rats treated with gentamicin did not change the protective effect of L-arginine. In rats receiving L-NAME alone, the level of BUN and creatinine and vasodilation to acetylcholine were not significantly different when compared to those of the control group, while relaxant responses to sodium nitroprusside and pinacidil were increased. These results suggest that gentamicin leads to an impairment in vascular smooth muscle relaxation in addition to acute tubular necrosis in the rat kidney. Supplementation of L-arginine has an important protective effect on gentamicin-induced nephropathy.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective Effect of <i>L</i>-Arginine Intake on the Impaired Renal Vascular Responses in the Gentamicin-Treated Rats

Seçilmiş¹,

Karataş²,

Yorulmaz³

et al. 2005

Nephron Physiol

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“…For example, it has been reported that use of polyaspartic acid prevented functional and histological changes of GSinduced nephrotoxicity (Gilbert et al, 1989). Administration of L-arginine (Can et al, 2000), melatonin , carvedilol and some medicinal plants such as arabic gum (AlMajed et al, 2002) ameliorate successfully GS-induced nephropathy. In another study, pretreatment with superoxide dismutase (8000 IU/kg) showed significant protection against GS-induced nephrotoxicity (Ali and Data are mean ± SE of six rats for each group.…”

Section: Histological Analysismentioning

confidence: 99%

Spirulina platensis protects against gentamicin‐induced nephrotoxicity in rats

Karadeniz

Yıldırım

Şimşek

et al. 2008

Phytotherapy Research

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The present study aimed to investigate the protective effect of Spirulina platensis (SP) on gentamicin sulphate (GS)-induced changes in the levels of lipid peroxidation and endogenous antioxidants in the kidney of rats. Sprague-Dawley rats were treated in separate groups as follows for 7 consecutive days: control (C), gentamicin sulphate (100 mg/kg i.p.) (GS), Spirulina platensis (1000 mg/kg orally) (SP) and Spirulina platensis (1000 mg/kg orally) plus gentamicin sulphate (100 mg/kg i.p.) (SP + GS). The degree of protection was evaluated by determining the effects of Spirulina platensis on malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPX) and nitric oxide (NO), and plasma creatinine and urea levels were estimated in kidney homogenates to evaluate antioxidant activity, and the kidney was histologically examined as well. Spirulina platensis elicited significant nephroprotective activity by decreasing lipid peroxidation (MDA) and elevated the levels of GSH, SOD, GPX, NO, creatinine and urea. Furthermore, these biochemical observations were supplemented by histological examination of the rat kidneys. In conclusion, the present study indicates a very important role of reactive oxygen species (ROS) and the relation to renal dysfunction and point to the therapeutic potential of Spirulina platensis in gentamicin sulphate induced nephrotoxicity.

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Comparative effects of selective and non-selective nitric oxide synthase inhibition in gentamicin-induced rat nephrotoxicity

Ghaznavi

Kadkhodaee

2006

Arch Toxicol

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Different nitric oxide synthase (NOS) isoforms are found in the kidney. Some studies provided evidences that increased endothelial NOS (eNOS) activity leads to restoration of renal function after injury, but activation of inducible NOS (iNOS) aggravates renal failure. In the present study, the beneficial effects of selective iNOS blockade in gentamicin (GM) induced nephrotoxicity have been investigated. Four groups of rats were studied. Untreated control rats received saline. In GM group, GM was injected (IV, 4 mg kg(-1)). In GM + L-NAME group rats received L-NAME (N-omega-L-arginine methyl ester, a non-selective NOS inhibitor) simultaneously with GM (IV, 30 mg kg(-1)). Additional doses of L-NAME were administered 2 and 4 h after GM (IP, 30 mg kg(-1)). In GM + L-NIL group rats were treated by N-imino-ethyl lysine (L-NIL, a selective iNOS inhibitor). First dose (IV, 3 mg kg(-1)) administrated simultaneously with GM. Next doses (IP, 3 mg kg(-1)) were administered 2 and 4 h after GM. In all groups, serum and urine creatinine levels were measured. Creatinine clearance was calculated and considered as an estimation of glomerular filtration rate (GFR). Urine N-acetyl-b-D-glucose aminidase (NAG) activities were also determined. After experiments, kidney sections were histologically studied. Selective iNOS inhibition by L-NIL prevented the GM-induced decrease in GFR and increase in creatinine levels, while complete non-selective NOS inhibition by L-NAME aggravated the GFR reduction, elevation of creatinine levels and enzyme release (P < 0.05). Histological studies showed that GM-treated kidneys had evidences of tubular damages and these damages were less evident by the administration of L-NIL. In conclusion, selective inhibition of iNOS may prevent GM-induced nephrotoxicity, whereas non-selective inhibition of NOS aggravates it.

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Protective effect of oral l-arginine administration on gentamicin-induced renal failure in rats

Cited by 38 publications

References 19 publications

Protective Effect of <i>L</i>-Arginine Intake on the Impaired Renal Vascular Responses in the Gentamicin-Treated Rats

Protective Effect of <i>L</i>-Arginine Intake on the Impaired Renal Vascular Responses in the Gentamicin-Treated Rats

Spirulina platensis protects against gentamicin‐induced nephrotoxicity in rats

Comparative effects of selective and non-selective nitric oxide synthase inhibition in gentamicin-induced rat nephrotoxicity

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