Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Pessoa, Edson Andrade; Convento, Márcia Bastos; Silva, R.G.; Oliveira, Andréia Silva de; Borges, Fernanda Teixeira; Schor, Nestor

doi:10.1590/s0100-879x2009005000005

Cited by 25 publications

(20 citation statements)

References 36 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: Discussionsupporting

confidence: 65%

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: Discussionsupporting

confidence: 65%

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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“…Cell viability was determined by exclusion of fluorescent dyes acridine orange and ethidium bromide (Sigma) (8) . In order to read viability were used only 10mL of the suspension of trypsinized cells that were mixed with 0.3 mL of the solution of acridine orange dye and ethidium bromide (100mg/ml) in a ratio v:v (1:1).…”

Section: Introductionmentioning

confidence: 99%

“…On the blade 5 mL was pipetted on the slide of Hoechst 33342 added to 5 mL of the cell suspension. The blade was stored for 10 minutes at room temperature and in the absence of light for chromatin staining (8) . Then the procedure was the count of 100 to 200 cells for each group.…”

Section: Introductionmentioning

confidence: 99%

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Nephrotoxicity Of Polymyxin B: Experimental Study In Cells And Implications For Nursing Practice

Neiva

Borges

Watanabe

et al. 2014

Rev. esc. enferm. USP

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RESUMENEl objetivo del estudio fue caracterizar los mecanismos de daño celular implicado en la fisiopatología de la citotoxicidad de la polimixina B en las células tubulares proximales (LLC-PK1) y discutir las propuestas de intervención de enfermería para identificar a los pacientes de riesgo y considerar la prevención o el tratamiento de la lesión renal aguda nefrotóxica. Corresponde a un estudio experimental cuantitativo in vitro, en el cual las células fueron expuestas a sulfato de polimixina B. La viabilidad celular se determinó por exclusión de los colorantes fluorescentes y el método morfológico con la visualización de cuerpos apoptóticos a la microscopía de fluorescencia. Las células expuestas a polimixina B demostraron reducción de la viabilidad, aumento de célu-las apoptóticas y mayor concentración de la enzima lactato deshidrogenasa. La administración de polimixina B in vitro demostró la necesidad de realizar acciones en la práctica clínica para minimizar los efectos adversos como la nefrotoxicidad. DESCRIPTORESPolimixina B Antibacterianos Lesión renal aguda Células LLC-PK1 Atención de enfermería RESUMOO objetivo do estudo foi caracterizar os mecanismos de lesão celular envolvidos na fisiopatologia da citotoxicidade da polimixina B em células tubulares proximais (LLC-PK1) e discutir as proposições de intervenção do enfermeiro para identificar os pacientes de risco e considerar a prevenção ou o tratamento para lesão renal nefrotóxica. Estudo experimental in vitro, onde as células foram expostas ao sulfato de polimixina B. A viabilidade celular foi determinada pela exclusão dos corantes fluorescentes e o método morfológico com visualização de corpos apoptóticos à microscopia de fluorescência. As células expostas à polimixina B apresentaram redução de viabilidade, aumento do número de células em apoptose e maior concentração da enzima desidrogenase láctea. A administração de polimixina B in vitro demonstrou a necessidade de ações na prática clínica para minimizar os efeitos adversos como a nefrotoxicidade. DESCRITORESPolimixina B Antibacterianos Lesão renal aguda Células LLC-PK1 Cuidados de enfermagem ABSTRACTThe aim of the study was to characterize the cell damage mechanisms involved in the pathophysiology of cytotoxicity of polymyxin B in proximal tubular cells (LLC -PK1) and discuss about the nurses interventions to identify at risk patients and consider prevention or treatment of nephrotoxicity acute kidney injury. This is a quantitative experimental in vitro study, in which the cells were exposed to 375μM polymyxin B sulfate concentration. Cell viability was determined by exclusion of fluorescent dyes and morphological method with visualization of apoptotic bodies for fluorescence microscopy. Cells exposed to polymyxin B showed reduced viability, increased number of apoptotic cells and a higher concentration of the enzyme lactate dehydrogenase. The administration of polymyxin B in vitro showed the need for actions to minimize adverse effects such as nephrotoxicity.

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“…The gentamicin is an aminoglycoside antibiotic widely used for the treatment of Gram-negative infections and is a well-known cause of renal failure, which occurs in 10-20% of patients receiving this drug (Pessoa et al, 2009;Ali, 1995;Bennett, 1986).…”

Section: Introductionmentioning

confidence: 99%

Kidney injury and cell therapy: Preclinical study

Cabral

Ferraz

Rizzo

et al. 2011

Microscopy Res & Technique

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The aim of this study is to show histological and immunofluorescence analysis of renal parenchyma of agoutis affected by gentamicin-induced renal disease after the infusion of bone marrow mononuclear cells (BMMC) stained with Hoechst®. Nine agouti's males were divided into three groups: Test group (TG): renal disease by gentamicin induced (n = 3), cell therapy group (CTG): renal disease by gentamicin induced and BMMC infusion (n = 3), and control group (CG): nonrenal disease and BMMC infusion (n = 3). TG and CTG were submitted to the protocol of renal disease induction using weekly application of gentamicin sulfate for 4 months. CG and CTG received a 1 × 108 BMMC stained with Hoechst and were euthanized for kidney examination 21 days after BMMC injection and samples were collected for histology and immunofluorescence analysis. Histological analysis demonstrated typical interstitial lesions in kidney similarly to human disease, as tubular necrosis, glomerular destruction, atrophy tubular, fibrotic areas, and collagen deposition. We conclude that histological analysis suggest a positive application of agouti's as a model for a gentamicin inducing of kidney disease, beyond the immunofluorescence analysis suggest a significant migration of BMMC to sites of renal injury in CTG.

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Gentamicin-induced preconditioning of proximal tubular LLC-PK1 cells stimulates nitric oxide production but not the synthesis of heat shock protein

Cited by 25 publications

References 36 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

Nephrotoxicity Of Polymyxin B: Experimental Study In Cells And Implications For Nursing Practice

Kidney injury and cell therapy: Preclinical study

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