The protective effect of taurine against gentamicin‐induced acute tubular necrosis in rats

Erdem, Ayşen; Gündoğan, Nimet Ünay; Usubütün, Alp; Kılınç, Kamer; Erdem, Remzi; Kara, Aysun; Bozkurt, Atilla

doi:10.1093/ndt/15.8.1175

Cited by 194 publications

(143 citation statements)

References 19 publications

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“…Researchers also observed that creatinine (Cr) level is a more accurate measurement for glomerular impairment than urea levels/Cr clearance. [42,43] Our study results coincide with earlier reports that a significant increase in plasma urea and creatinine or decrease in potassium levels [40,41,44] might indicate a nephrotoxic condition in GEN-treated rats and may be due to kidney damage caused by the enhanced generation of ROS. These findings correlated well with the renal histological examination, which revealed renal tubular necrosis and interstitial nephritis.…”

Section: Discussionsupporting

confidence: 91%

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Nephroprotective Effect ofWithania somnifera:A Dose-Dependent Study

Jeyanthi

Subramanian

2009

Renal Failure

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In the present study, we investigated the protective effect of Withania somnifera, an indigenous medicinal herb used in ayurvedic traditional systems for more than 3000 years in India, on gentamicin (GEN)-induced nephrotoxicity. The root extract of three different doses of W. somnifera (viz., 250, 500, and 750 mg/kg) was administered orally to rats for 14 days before GEN treatment and thereafter concurrently with GEN (100 mg/kg) for 8 days. Nephrotoxicity was evident in GEN-treated rats by significant increase in kidney weight, urea, creatinine, urinary protein, and glucose, and significant reduction in body weights and potassium, which was histopathologically confirmed by tubular necrosis. In contrast W. somnifera (500 mg/kg) significantly reversed these changes as evidenced microscopically when compared to other two doses of W. somnifera (250 and 750 mg/kg), and there were no significant changes in the levels of sodium in the experimental animals compared to control. Thus, our results suggested the nephroprotective effect of Withania somnifera, which could be by enhancing antioxidant activity with natural antioxidants and scavenging the free radicals.

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Section: Discussionsupporting

confidence: 91%

“…[1] The present study confirmed that GEN at a dose of 100 mg/kg b.w for eight days produces nephrotoxicity, [40,41] as evidenced by the impairment in glomerular function. Researchers also observed that creatinine (Cr) level is a more accurate measurement for glomerular impairment than urea levels/Cr clearance.…”

Section: Discussionsupporting

confidence: 84%

Nephroprotective Effect ofWithania somnifera:A Dose-Dependent Study

Jeyanthi

Subramanian

2009

Renal Failure

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“…Support for the concept of distinctly different responses to aminoglycosides in vivo and in vitro also exists for their nephrotoxic side effects. Tubular necrosis is a confirmed route of cell death in vivo 24 while renal cell lines show apoptosis in response to aminoglycosides. 25 Multiple organelles are involved in the ototoxic cascade following chronic administration of aminoglycosides.…”

Section: Discussionmentioning

confidence: 99%

Caspase-independent pathways of hair cell death induced by kanamycin in vivo

et al. 2005

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Cochlear and vestibular sensory cells undergo apoptosis when exposed to aminoglycoside antibiotics in organ culture, but mechanisms of chronic drug-induced hair cell loss in vivo are unclear. We investigated cell death pathways in a mouse model of progressive kanamycin-induced hair cell loss. Hair cell nuclei showed both apoptotic-and necrotic-like appearances but markers for classic apoptotic pathways (cytochrome c, caspase-9, caspase-3, JNK, TUNEL) were absent. In contrast, drug treatment caused EndoG translocation, activation of l-calpain, and both the synthesis and activation of cathepsin D. Poly (ADP-ribose) polymerase 1 (PARP1) was decreased, but a caspase-derived 89 kDa PARP1 fragment was not present. The mRNA level of PARP1 remained unchanged. Thus, chronic administration of aminoglycosides causes multiple forms of cell death, without a major contribution by classic apoptosis. These results provide a better understanding of the toxic effects of aminoglycosides and are relevant to design protection from aminoglycosideinduced hearing loss.

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“…The blood analyses were done by Meril's auto-analyser. [17][18][19] (Merilyzer Auto-Quant 100); this is a fully automatic biochemical analyser.…”

Section: Methodsmentioning

confidence: 99%