The protective effect of melatonin on adriamycin-induced acute cardiac injury


Koçak G., Erbil K. M., ÖZDEMİR İ., AYDEMİR S., Sunar B., Tuncel M., ...Daha Fazla

Canadian Journal of Cardiology, cilt.19, sa.5, ss.535-541, 2003 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 19 Sayı: 5
  • Basım Tarihi: 2003
  • Dergi Adı: Canadian Journal of Cardiology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.535-541
  • Anahtar Kelimeler: Adriamycin, Cardiotoxicity, Electron microscopy, Free radicals, Melatonin
  • Lokman Hekim Üniversitesi Adresli: Hayır

Özet

Background: Cardiotoxicity is the main complication of adriamycin (ADR), which is a widely used chemotherapeutic agent. Objective: To examine the potential cardioprotective effect of melatonin (MEL) on acute ADR cardiotoxicity in a rat model. Methods: Cardioprotection was assessed on the basis of myocardial lipid peroxidation and ultrastructure. Rats were given MEL at a daily dose of 5 mg/kg and ADR 15 mg/kg, intraperitoneally. The MEL-1 group rats received one dose and the MEL-7 group rats six daily doses of MEL and were sacrificed at the end of one and seven days, respectively. Rats in the ADR-1 and ADR-7 groups were each given a single dose of ADR, and were then sacrificed 24 h and seven days later, respectively. The MEL+ADR-1 group rats received one dose each of ADR and MEL simultaneously and were sacrificed 24 h later. The MEL+ADR-7 group received a single dose of ADR plus a daily MEL dose for six consecutive days, and were sacrificed seven days after the ADR injection. Reswults: Lipid peroxidation products were elevated in both ADR-1 and ADR-7 groups, and this elevation was significantly inhibited by MEL treatment. Electron microscopy confirmed that ADR was positively cardiotoxic after one and seven days of exposure. The extent of ADR-induced myocardial damage was markedly reduced when MEL was combined with ADR (MEL+ADR-1 and MEL+ADR-7). Conclusion: The results suggest that MEL is highly efficacious at reducing the acute cardiotoxic effects of high dose ADR, and that it acts by preventing lipid peroxidation.