Reduction of cisplatin hepatotoxicity by procainamide hydrochloride in rats

Antonio Zicca, Sergio Cafaggi, Maria A. Mariggiò, Maria O. Vannozzi, Massimo Ottone, Vittorio Bocchini, Gabriele Caviglioli, Maurizio Viale

Research output: Contribution to journalArticlepeer-review


In preceding papers, we proposed that procainamide hydrochloride, a class I antiarrhythmic agent, was able to protect mice and rats from cisplatin-induced nephrotoxicity and that it could exert its action through accumulation in kidneys followed by coordination with cisplatin (or its hydrolysis metabolites) and formation of a less toxic platinum compound similar to the new platinum(II) triamine complex cis-diamminechloro-[2-(diethylamino)ethyl 4-amino-benzoate, N4]-chlorideplatinum(II) monohydrochloride monohydrate, obtained by the reaction of cisplatin with procaine hydrochloride. Hepatotoxicity is not considered as a dose-limiting toxicity for cisplatin, but liver toxicity can occur when the antineoplastic drug is administered at high doses. Here, we report that procainamide hydrochloride, at an i.p. dose of 100 mg/kg, reduces cisplatin-induced hepatotoxicity, as evidenced by the normalization of plasma activity of glutamic oxalacetic transaminase and γ-glutamyl transpeptidase, as well as by histological examination of the liver tissue. Twenty-four hours after i.p. treatment with the combination of 7.5 mg/kg cisplatin and 100 mg/kg procainamide, a significant increase of procainamide (+56%, P

Original languageEnglish
Pages (from-to)265-272
Number of pages8
JournalEuropean Journal of Pharmacology
Issue number3
Publication statusPublished - May 10 2002


  • Cisplatin
  • Hepatotoxicity
  • Procainamide
  • Protection

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology


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