Differential roles of dihydropyridine calcium antagonist nifedipine, nitrendipine and amlodipine on gentamicin-induced renal tubular toxicity in rats

Jin, Li; Li, Qixiong; Xie, Xianhong; Ao, Ying; Tie, Chaorong; Song, Ren‐Jie

doi:10.1016/j.ejphar.2009.08.021

Cited by 70 publications

(35 citation statements)

References 32 publications

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“…‫,ء‬ p Ͻ 0.05; ‫,ءء‬ p Ͻ 0.01. creased after a 24-h exposure to cisplatin and gentamicin, although the mRNA level was significantly increased after exposure to ethylene glycol as shown previously (Hosohata et al, 2011). Cisplatin (Lieberthal et al, 1998) and gentamicin (Li et al, 2009;Pessoa et al, 2009) are known to directly cause renal cell death, whereas the toxicity of ethylene glycol is low (Poldelski et al, 2001). Ethylene glycol-induced renal toxicity is caused by the accumulation of its metabolites (Poldelski et al, 2001) and/or obstruction of renal tubules by the metabolite-related crystals (Hackett et al, 1990).…”

Section: Discussionmentioning

confidence: 88%

Urinary Vanin-1 As a Novel Biomarker for Early Detection of Drug-Induced Acute Kidney Injury

Hosohata

Ando²,

Fujimura³

2012

J Pharmacol Exp Ther

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Drug-induced nephrotoxicity is a serious problem in patients with hospital-acquired acute kidney injury (AKI). A new renal biomarker is needed because traditional markers are not sensitive for early detection of drug-induced AKI. In a recent study, we demonstrated that vanin-1 is a novel candidate biomarker of nephrotoxicant-induced kidney injury. The objective of the present study is to determine whether the increase in urinary vanin-1 is detected before the elevations of serum creatinine or urinary N-acetyl-␤-glucosaminidase (NAG), kidney injury molecule-1 (Kim-1), and neutrophil gelatinase-associated lipocalin (NGAL) in the two well established animal models of drug-induced AKI. After the administration of a higher dose of cisplatin (10 mg/kg, a single intraperitoneal dose) or gentamicin (120 mg/kg per day, once daily intraperitoneal dose for 9 days), urinary vanin-1 was detected earlier than the other biomarkers. In rats treated with a lower dose of cisplatin (5 mg/kg, a single intraperitoneal dose) or gentamicin (40 mg/kg per day, once daily intraperitoneal dose for 9 days), serum creatinine and urinary NAG were not changed throughout the study period, whereas urinary vanin-1, Kim-1, and NGAL were significantly increased. The renal vanin-1 protein levels were significantly decreased in rats treated with the higher dose of cisplatin on day 5 and gentamicin on day 9, and the immunofluorescence analyses confirmed that vanin-1 immunoreactivity in tubular cells was reduced with the time after the dose of cisplatin, indicating that urinary vanin-1 was leaked from tubular cells. These results suggest that, compared with urinary Kim-1 and NGAL, urinary vanin-1 is an earlier and equally sensitive biomarker for drug-induced AKI.

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Section: Discussionmentioning

confidence: 88%

Urinary Vanin-1 As a Novel Biomarker for Early Detection of Drug-Induced Acute Kidney Injury

Hosohata

Ando²,

Fujimura³

2012

J Pharmacol Exp Ther

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“…Recently, Li et al demonstrated that amlodipine decreased the production of MDA and increased antioxidants, such as SOD and GSH, in gentamicin-induced renal-tubular toxicity in rats. [35].…”

Section: Discussionmentioning

confidence: 99%

The Effects of Amlodipine on the Biochemical and Histopathological Changes in the Rabbit Ileum Subjected to Ischemia-Reperfusion

Coşkun¹,

Günal²,

Halıcı³

et al. 2011

EAJM

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Objective: The aim of this study was to determine the potential, protective effects of amlodipine in an experimental, ischemia-reperfusion (I/R) model in the rabbit small intestine. Materials and Methods:The rabbits were divided into four groups: sham-operated, amlodipine (10 mg/kg) + sham-operated, I/R, and I/R + amlodipine (10 mg/kg) groups. An intestinal I/R model was applied to the rabbits. The superior mesenteric artery was occluded for 1 h with an atraumatic vascular clamp and then was reperfused for 2 h. Animals in the amlodipine and I/R + amlodipine groups received the amlodipine by oral gavage. At the end of the 2-h-reperfusion period, the animals were sacrificed.Results: Pretreatment with amlodipine significantly increased SOD activity and GSH levels to values close to those found in the serum from the I/R group. Rabbits in the I/R group showed high levels of serum MDA. Amlodipine pretreatment significantly reduced the serum MDA levels compared to the I/R group, although the MDA levels in the I/R + amlodipine group were still higher than in the sham-operated group. The I/R damage was ameliorated by amlodipine pretreatment, as evidenced by histopathological analysis. Conclusion:The present study is the first to report an attenuation of I/Rinduced intestinal injury by the systemic administration of amlodipine.Key Words: Amlodipine, Ischemia-Reperfusion, Glutathione, Superoxide Dismutase, Malonyldialdehyde, Rabbit Özet Amaç: Biz bu çalışmada, tavşan ince barsak iskemi-reperfüzyon (I/R) deneysel modeli üzerine amlodipin'in koruyucu etkisini inceledik. Gereç ve Yöntem:Tavşanlar dört guruba ayrıldı: şam operasyon gurubu, 10mg/kg amlodipin+şam operasyon gurubu, I/R gurubu, I/R+ 10 mg/kg amlodipin gurubu. İntestinal iskemi/reperfüzyon modeli tavşanlara uygulanıldı. Superior mezenterik arter 1 saat sure ile atravmatik vasküler klemp ile klempe edildi sonrasında 2 saat reperfüzyon uygulanıldı. Amlodipin ve amlodipin+I/R guruplarına oral gavaj ile amlodipin verildi. İki saatlik reperfüzyon süresinin sonunda hayvanlar sakrifiye edildi. I/R hasarının amlodipin uygulaması ile düzeldiği histopatolojik analizler ile ispatlandı. Bulgular: Amlodipin uygulaması I/R 'da serumda bulunan SOD aktivitesi ve GSH seviyesini anlamlı şekilde artırdı. Tavşanlarda intestinal I/R'ında yüksek seviyede MDA gözlendi. Amlodipin uygulaması intestinal I/R bulunan tavşan serumunda MDA aktivite seviyesini anlamlı şekilde düşürürken bu düşüş I/R+amlodipin gurubu control gurubu ile mukayese edildiğinde çok daha fazlaydı. Sonuç:Mevcut çalışma I/R ile oluşan intestinal hasar üzerine amlodipin'in sistemik uygulamasının iyleştirici etkisini gösteren ilk çalışmadır.

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“…The effects of dihydropyridine calcium antagonist-NIT on membrane lipid peroxidation indicate that it inhibits peroxidation by intercepting oxy-and/or lipid-free radical intermediates. These data raise the possibility that antiperoxidant action may contribute to the spectrum of pharmacology and therapeutic activities of dihydropiridine Ca 2+ antagonists (Li et al, 2009).…”

Section: Resultsmentioning

confidence: 98%

Influence of dihydropyridine calcium antagonist nitrendipine on benzo(a)pyrene-induced oxidative stress

2011

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The aim of this study was to investigate the influence of nitrendipine (NIT), a dihydropyridine derived calcium channel antagonist, on polycyclic aromatic hydrocarbon benzo(a)pyrene (BAP)-induced oxidative stress. Male Sprague Dawley rats (155-220 g) were divided into four groups: Control (corn oil, i.p.); BAP (200 mg/kg, i.p.), BAP + NIT (200 mg/kg, i.p. + 50 mg/kg, i.p.), and NIT (50 mg/kg, i.p.) groups. Twenty-four hours after the injection of BAP, the rats were sacrificed and blood samples, liver, lung, and brain tissues were removed to determine serum alanine transaminase (ALT), aspartate transferase (AST), and gamma-glutamyltransferase (GGT) activities and tissue thiobarbituric acid reactive substances (TBARS), glutathione (GSH), and superoxide dismutase (SOD) levels. BAP significantly elevated serum ALT and TBARS levels in all tissues. However, NIT pre-treatment protected against increasing TBARS levels in lung and brain tissues. In addition, NIT pre-treatment significantly increased SOD levels in lung and liver tissues, as well as GSH levels in the lungs, compared to the BAP group. Thus, in conclusion, further studies are required to confirm the protective effects of calcium channel blockers, especially in liver tissue.

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Differential roles of dihydropyridine calcium antagonist nifedipine, nitrendipine and amlodipine on gentamicin-induced renal tubular toxicity in rats

Cited by 70 publications

References 32 publications

Urinary Vanin-1 As a Novel Biomarker for Early Detection of Drug-Induced Acute Kidney Injury

Urinary Vanin-1 As a Novel Biomarker for Early Detection of Drug-Induced Acute Kidney Injury

The Effects of Amlodipine on the Biochemical and Histopathological Changes in the Rabbit Ileum Subjected to Ischemia-Reperfusion

Influence of dihydropyridine calcium antagonist nitrendipine on benzo(a)pyrene-induced oxidative stress

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