Abstract
Cisplatin is a widely used antineoplastic drug. Major drawback of cisplatin therapy is its nephrotoxicity. The objective of this study was to check the effect of tannic acid on cisplatin induced nephrotoxicity. Post-treatment of tannic acid prevents cisplatin (5mg/kg) induced nephrotoxicity and decreases poly(ADP-ribose) polymerase cleavage, phosphorylation of p38 and hypoacetylation of histone H4. In contrast, co-treatment of tannic acid potentiates the nephrotoxicity. Comparative nephrotoxicity studies show that co-treatment of tannic acid with reduced dose of cisplatin (1.5mg/kg) developed almost similar nephrotoxicity. MALDI protein profiling of plasma samples provides indirect evidence that tannic acid co-treatment increases bioavailability of cisplatin.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acetylation / drug effects
-
Animals
-
Antineoplastic Agents / toxicity*
-
Blood Proteins / chemistry
-
Blood Urea Nitrogen
-
Body Weight / drug effects
-
Cisplatin / toxicity*
-
Creatinine / blood
-
Dose-Response Relationship, Drug
-
Histones / metabolism
-
Kidney / drug effects
-
Kidney / enzymology
-
Kidney / pathology
-
Kidney Diseases / chemically induced*
-
Kidney Diseases / pathology*
-
Male
-
Phosphorylation / drug effects
-
Poly(ADP-ribose) Polymerases / metabolism
-
Protein Processing, Post-Translational / drug effects
-
Rats
-
Rats, Sprague-Dawley
-
Serum Albumin
-
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
-
Tannins / pharmacology*
-
p38 Mitogen-Activated Protein Kinases / metabolism
Substances
-
Antineoplastic Agents
-
Blood Proteins
-
Histones
-
Serum Albumin
-
Tannins
-
Creatinine
-
Poly(ADP-ribose) Polymerases
-
p38 Mitogen-Activated Protein Kinases
-
Cisplatin