Protective effect of L-carnitine against cisplatin-induced liver and kidney oxidant injury in rats

Çayır K., Karadeniz A., Yildirim A., Kalkan Y., Karakoç A., Keleş M., ...Daha Fazla

CENTRAL EUROPEAN JOURNAL OF MEDICINE, cilt.4, sa.2, ss.184-191, 2009 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 4 Sayı: 2
  • Basım Tarihi: 2009
  • Doi Numarası: 10.2478/s11536-009-0021-x
  • Dergi Adı: CENTRAL EUROPEAN JOURNAL OF MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.184-191
  • Anahtar Kelimeler: L-carnitine, Cisplatin, Liver, Kidney, Oxidative damage, PROPIONYL-L-CARNITINE, ACUTE-RENAL-FAILURE, INDUCED OXIDATIVE DAMAGE, INDUCED HEPATOTOXICITY, SUPEROXIDE-DISMUTASE, LIPID-PEROXIDATION, ELLAGIC ACID, VITAMIN-E, GLUTATHIONE, TISSUES
  • Atatürk Üniversitesi Adresli: Evet

Özet

The present study was designed to investigate the protective effects of L-carnitine (LC) on changes in the levels of lipid peroxidation and endogenous antioxidants induced by cisplatin (cis-diamminedichloroplatinum II, CDDP) in the liver and kidney tissues of rats. Twenty-four Sprague Dawley rats were equally divided into four groups of six rats each: control, cisplatin, L-carnitine, and L-carnitine plus cisplatin. The degree of protection produced by L-carnitine was evaluated by determining the level of malondialdehyde (MDA). The activity of glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and superoxide dismutase (SOD) were estimated from liver and kidney homogenates, and the liver and kidney were histologically examined as well. L-carnitine elicited significant liver and kidney protective activity by decreasing the level of lipid peroxidation (MDA) and elevating the activity of GSH, GSHPx, GST, and SOD. Furthermore, these biochemical observations were supported by histological findings. In conclusion, the present study indicates a significant role for reactive oxygen species (ROS) and their relation to liver and kidney dysfunction, and points to the therapeutic potential of LC in CDDP-induced liver and kidney toxicity.