Effect of N&lt;sup&gt;G&lt;/sup&gt;-Nitro-&lt;i&gt;L&lt;/i&gt;·Arginine Methyl Ester on Nephrotoxicity Induced by Gentamicin in Rats

Rivas-Cabañero, Lina; Rodríguez-Barbero, Alicia; Arévalo, Miguel; López‐Novoa, José M.

doi:10.1159/000188713

Cited by 22 publications

(9 citation statements)

References 8 publications

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“…The inhibition of NO production exacerbates GM nephrotoxicity suggesting that the enhancement of NO production is very important to prevent exacerbation of renal damage in GM-induced nephrotoxicity [37,38]. On the other hand, NO is able to react with O 2 - to produce peroxynitrite anion which itself is very toxic [39,40].…”

Section: Discussionmentioning

confidence: 99%

S-allylmercaptocysteine scavenges hydroxyl radical and singlet oxygen in vitro and attenuates gentamicin-induced oxidative and nitrosative stress and renal damage in vivo

et al. 2004

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BackgroundOxidative and nitrosative stress have been involved in gentamicin-induced nephrotoxicity. The purpose of this work was to study the effect of S-allylmercaptocysteine, a garlic derived compound, on gentamicin-induced oxidative and nitrosative stress and nephrotoxicity. In addition, the in vitro reactive oxygen species scavenging properties of S-allylmercaptocysteine were studied.ResultsS-allylmercaptocysteine was able to scavenge hydroxyl radicals and singlet oxygen in vitro. In rats treated with gentamicin (70 mg/Kg body weight, subcutaneously, every 12 h, for 4 days), renal oxidative stress was made evident by the increase in protein carbonyl content and 4-hydroxy-2-nonenal, and the nitrosative stress was made evident by the increase in 3-nitrotyrosine. In addition, gentamicin-induced nephrotoxicity was evident by the: (1) decrease in creatinine clearance and in activity of circulating glutathione peroxidase, and (2) increase in urinary excretion of N-acetyl-β-D-glucosaminidase, and (3) necrosis of proximal tubular cells. Gentamicin-induced oxidative and nitrosative stress and nephrotoxicity were attenuated by S-allylmercaptocysteine treatment (100 mg/Kg body weight, intragastrically, 24 h before the first dose of gentamicin and 50 mg/Kg body weight, intragastrically, every 12 h, for 4 days along gentamicin-treatment).ConclusionIn conclusion, S-allylmercaptocysteine is able to scavenge hydroxyl radicals and singlet oxygen in vitro and to ameliorate the gentamicin-induced nephrotoxicity and oxidative and nitrosative stress in vivo.

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Section: Discussionmentioning

confidence: 99%

S-allylmercaptocysteine scavenges hydroxyl radical and singlet oxygen in vitro and attenuates gentamicin-induced oxidative and nitrosative stress and renal damage in vivo

et al. 2004

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“…It inhibits all three isoforms of NOS, and experimental data indicate that ADMA produces the expected physiologic changes when infused in vivo (1,13,14). Furthermore, animal models have shown that other NOS inhibitors enhance atherogenesis and promote renal damage consequent upon reduced NO generation (15,16). However, the absolute levels of ADMA and the differences between groups in the current clinical studies are small.…”

mentioning

confidence: 84%

Asymmetric Dimethylarginine and Kidney Disease—Marker or Mediator?

Vallance¹,

Leiper²

2005

Journal of the American Society of Nephrology

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“…Excess NO production has also been reported in gentamicin-induced acute renal failure [38]. However, NO may play a protective role against drug-induced nephrotoxicity as inhibition of NOS by L-NAME has been shown to both aggravate gentamicin-induced renal failure and enhance acute cyclosporin nephrotoxicity [39].…”

Section: Nitric Oxide the Kidney And Renal Diseasementioning

confidence: 99%

Cytokine-Stimulated Nitric Oxide Production in the Human Renal Proximal Tubule and Its Modulation by Natriuretic Peptides: A Novel Immunomodulatory Mechanism?

Chatterjee

Hawksworth²,

McLay³

1999

Nephron Exp Nephrol

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Although the importance of the human kidney in a variety of disease states is well recognised, the exact mechanisms involved remain unclear. Animal disease models suggest that while high local concentrations of nitric oxide (NO) may play a key role in the initiation and progression of renal disease, low levels may also be essential for normal renal function and cell protection, possibly explaining the variable reports of both beneficial and detrimental responses of renal disease models following NO inhibition. NO has both physiological and pathological roles and clearly a balance between these two primary roles is likely to prevail leading to the conclusion that partial rather than total inhibition of NO production may be beneficial. Despite increasing evidence for the role of NO from animal disease models, little is known of the role of NO and potential modulators within the human kidney. In this review we describe three series of studies during which we examined the ability of primary cultures of human proximal tubular cells to produce NO in response to inflammatory cytokines and the possible role of potential modulators such as the natriuretic peptides. Following challenge with the combination of inflammatory cytokines IL-1β, TNF-α, and IFN-γ, such cultures exhibit a time-dependent increase in inducible NO synthetase induction and corresponding NO production, an effect which was inhibited by L-NMMA. In the second series of studies we demonstrated that increasing concentrations of atrial natriuretic factor (ANF) or C_(4–23)ANF could stimulate a time- and concentration-dependent increase in nitric oxide production which was again abolished by L-NMMA. These results suggested that ANF acting at the natriuretic peptide receptor C could stimulate nitric oxide production in human proximal tubular cells. In the final series of studies we demonstrated that pro-inflammatory cytokine-induced nitric oxide production could be inhibited by ANF, brain natriuretic peptide, C-type natriuretic peptide or C_(4–23)ANF. The actions of the natriuretic peptides and C_(4–23)ANF was to return pro-inflammatory nitric oxide production to those observed when human proximal tubular cells were incubated with ANF alone indicating that this inhibition was mediated via the natriuretic peptide receptor C. The function of NO in the kidney is unclear but undoubtedly it has both beneficial and detrimental actions which in health remain in balance. However, when the kidney is subjected to an immune challenge, high cytotoxic levels of NO are produced locally and appear to be responsible for local damage, unfortunately total inhibition of NO production during such disease states does not always result in benefit. Clearly total abolition of an NO response removes important integral protective actions such as vasodilation. In the ideal situation, treatment of disease processes related to NO excess would involve the inhibition of these high local levels while still protecting vital dependent mechanisms. We believe that th...

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Effect of N<sup>G</sup>-Nitro-<i>L</i>·Arginine Methyl Ester on Nephrotoxicity Induced by Gentamicin in Rats

Cited by 22 publications

References 8 publications

S-allylmercaptocysteine scavenges hydroxyl radical and singlet oxygen in vitro and attenuates gentamicin-induced oxidative and nitrosative stress and renal damage in vivo

S-allylmercaptocysteine scavenges hydroxyl radical and singlet oxygen in vitro and attenuates gentamicin-induced oxidative and nitrosative stress and renal damage in vivo

Asymmetric Dimethylarginine and Kidney Disease—Marker or Mediator?

Cytokine-Stimulated Nitric Oxide Production in the Human Renal Proximal Tubule and Its Modulation by Natriuretic Peptides: A Novel Immunomodulatory Mechanism?

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