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Effect of fructose-1,6-bisphosphate on the nephrotoxicity induced by cisplatin in rats.
- Source :
-
Inflammation [Inflammation] 2011 Feb; Vol. 34 (1), pp. 67-71. - Publication Year :
- 2011
-
Abstract
- Cisplatin is one of the most active cytotoxic agents in the treatment of cancer, but its clinical use is frequently limited by nephrotoxicity. The study presented here attempted to evaluate the effect of fructose-1,6-bisphosphate in the cisplatin-induced nephrotoxicity in rats. The drugs were administered intraperitoneally as a single dose: sodium chloride 0.9%, cisplatin (6 mg/kg), fructose-1,6-bisphosphate (500 mg/kg), and cisplatin plus fructose-1,6-bisphosphate (6 and 500 mg/kg, respectively). The use of cisplatin resulted in significant elevation of serum creatinine and urea. The group that received cisplatin plus fructose-1,6-bisphosphate presented a significantly lower level of creatinine and urea compared to the cisplatin group. Acute tubular necrosis was demonstrated in the animals that received cisplatin and a less severe one in the cisplatin plus fructose-1,6-bisphosphate group. Fructose-1,6-bisphosphate has a protective effect over renal function and renal parenchyma in a rat experimental model of cisplatin-induced nephrotoxicity. The anti-inflammatory effect of fructose-1,6-bisphosphate confirms its protective effect in cases of cellular injury.
- Subjects :
- Acute Kidney Injury chemically induced
Acute Kidney Injury prevention & control
Animals
Creatinine blood
Cytoprotection
Fructosediphosphates administration & dosage
Kidney pathology
Kidney Tubular Necrosis, Acute prevention & control
Male
Necrosis
Nitric Oxide blood
Nitric Oxide Synthase genetics
Rats
Rats, Wistar
Urea blood
Weight Loss drug effects
Cisplatin toxicity
Fructosediphosphates pharmacology
Kidney drug effects
Kidney Tubular Necrosis, Acute chemically induced
Subjects
Details
- Language :
- English
- ISSN :
- 1573-2576
- Volume :
- 34
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Inflammation
- Publication Type :
- Academic Journal
- Accession number :
- 20419391
- Full Text :
- https://doi.org/10.1007/s10753-010-9212-5