Does gentamicin induce acute renal failure by increasing renal TXA2 synthesis in rats?

Papanikolaou, Nikolaos; Peros, George; Morphake, P.; Gkikas, G.; Maraghianne, D.; Tsipas, G.; Kostopoulos, Konstantinos; C, Arambatze; El, Gkika; Bariéty, J

doi:10.1016/0952-3278(92)90229-c

Cited by 27 publications

(18 citation statements)

References 19 publications

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“…Papanikolaou et al, 28 reported that gentamicin is incorporated and accumulated in proximal tubule lysosomes which explain the gentamicininduced nephrotoxicity.…”

Section: 23mentioning

confidence: 99%

Renoprotective and anti-oxidant effects of coleus forskohlii against gentamicin induced nephrotoxicity in albino wistar rats

Fatima¹,

Sultana²

2018

actapharm

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The aim of present study was to evaluate the protective effects of Coleus forskohlii against Gentamicin (GM)-induced nephrotoxicity in male albino wistar rats.Thirty rats were divided into five groups (n=6). Control rats received normal saline. Nephrotoxicity was induced in rats by gentamicin (80mg/Kg, IP) and treated with Silymarin (100mg/Kg, p.o,), aqueous and ethanolic extracts of (500mg/Kg, p.o) C. Forskohlii respectively for 15days. Markers of renal function (urea, uric acid and Creatinine), antioxidant markers were evaluated along with histopathological investigation in all experimental groups. GM-treated rats showed significant increase in serum levels of renal markers, TBARS and decrease in GSH, SOD, CAT. Histopathological examinations of GMtreated rats revealed degenerative changes in glomeruli and renal tubules. Administration of aqueous and ethanolic root extracts of Coleus forskohlii, protected the kidney tissues against toxic effects of gentamicin as evidenced by amelioration of histopathological changes and normalization of kidney biochemical parameters.The results of present study confirm the nephroprotective and anti-oxidant activity of C. forskohlii.

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“…Papanikolaou et al, 28 reported that gentamicin is incorporated and accumulated in proximal tubule lysosomes which explain the gentamicininduced nephrotoxicity.…”

Section: 23mentioning

confidence: 99%

Renoprotective and anti-oxidant effects of coleus forskohlii against gentamicin induced nephrotoxicity in albino wistar rats

Fatima¹,

Sultana²

2018

actapharm

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“…Clinically, it was reported that urinary excretion of TXB 2 was increased 4.5-fold during and immediately after cisplatin infusion in patients treated for various malignancies. 31 TXA 2 production was also observed following treatment with other cytotoxic drugs such as gentamicin 32 and cyclosporine. 33 This further supports the clinical relevance of our findings and implies that not only might a defective TP-Siva axis contribute to apoptosis resistance in tumours, but a functional TP-Siva axis in surrounding normal tissues and organs might also contribute to the toxicity of the chemotherapeutic treatment.…”

Section: Discussionmentioning

confidence: 82%

Thromboxane A2 modulates cisplatin-induced apoptosis through a Siva1-dependent mechanism

Iorio-Morin

Germain

et al. 2012

Cell Death Differ

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Thromboxane A 2 (TXA 2 ) is an important lipid mediator whose function in apoptosis is the subject of conflicting reports. Here, a yeast two-hybrid screen for proteins that interact with the C-terminus of the TXA 2 receptor (TP) identified Siva1 as a new TP-interacting protein. Contradictory evidence suggests pro-and anti-apoptotic roles for Siva1. We show that a cisplatin treatment induces TXA 2 synthesis in HeLa cells. We demonstrate that endogenous TP stimulation promotes cisplatin-induced apoptosis of HeLa cells and that such modulation requires the expression of Siva1, as evidenced by inhibiting its endogenous expression using siRNAs. We reveal that, upon stimulation of TP, degradation of Siva1 is impeded, resulting in an accumulation of the protein, which translocates from the nucleus to the cytosol. Translocation of Siva1 correlates with its reduced interaction with Mdm2 (an inhibitor of p53 signalling), as well as with its increased interaction with TRAF2 and XIAP (known to enhance pro-apoptotic signalling). Our data provide a model that reconciles the pro-and anti-apoptotic roles that were reported for Siva1 and identify a new mechanism for promoting apoptosis by G protein-coupled receptors. Our findings may have implications in the use of cyclo-oxygenase inhibitors during cisplatin chemotherapy and might provide a target to reduce cisplatin toxicity on non-cancerous tissues.

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“…Simultaneously with the proliferative effect, gentamicin induces mesangial cell apoptosis in renal glomeruli and cultured mesangial cells [1]. Mechanisms of gentamicin nephrotoxicity include several ways: Gentamicin enhances the production of hydroxyradicals [19]; increases in the renal cortical phospholipidosis [20]; gentamicin inhibits Na + -K + -ATPase in renal tubule cells [21]; thromboxane A2 (TXA 2 ) and prostaglandins (PGE) increasing [22]; effect on renal protein synthesis [23]; lysosomal [24] and mitochondrial injury [25]. Combination of these effects could induce acute renal failure [26].…”

Section: Resultsmentioning

confidence: 99%

In Vitro Assessment of Gentamicin Cytotoxicity on the Selected Mammalian Cell Line (Vero cells)

Kováčik

Tvrdá

Fülöpová

et al. 2017

Advanced Research in Life Sciences

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The aim of this study was to evaluate the in vitro cytotoxicity of different concentrations (500-7500 μg/mL) of gentamicin -GENT (aminoglycoside antibiotic) on the selected mammalian cell line (Vero -cell line from African green monkey kidney). Analysis of the cell morphological changes was microscopically evaluated (magnification x 400). Quantification of Ca, Mg and total proteins was performed using spectrophotometry on device Rx Monza (Randox). Quantification of Na, K and Cl was performed on the automatic analyzer EasyLyte. The cell viability was assessed using the metabolic mitochondrial MTT test. Vero cells were able to survive at concentrations of 500 (89.21 %), 1000 (79.54 %) and 2000 μg/mL (34.59 %). We observed statistically significant decrease of vital cell content at concentrations of 2000, 4500, 7500 μg/mL against control group. Vero cell line slightly reacted to the presence of GENT but total proteins and mineral parameters were not significantly affected. Vero cells were highly sensitive to GENT with a significant decrease of viability at concentrations of 2000 and 4500 μg/mL (P < 0.001). Our data reveal that GENT has a significant cytotoxic and adverse effect on the cell viability.

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Does gentamicin induce acute renal failure by increasing renal TXA2 synthesis in rats?

Cited by 27 publications

References 19 publications

Renoprotective and anti-oxidant effects of coleus forskohlii against gentamicin induced nephrotoxicity in albino wistar rats

Renoprotective and anti-oxidant effects of coleus forskohlii against gentamicin induced nephrotoxicity in albino wistar rats

Thromboxane A2 modulates cisplatin-induced apoptosis through a Siva1-dependent mechanism

In Vitro Assessment of Gentamicin Cytotoxicity on the Selected Mammalian Cell Line (Vero cells)

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