Effects of L-carnitine on kidney histopathology, plasma and tissue total sialic acid, malondialdehyde and glutathione concentrations in response to gentamicin administration in Balb/C mice


KART A., YAPAR K., KARAPEHLIVAN M., TUNCA R., OGUN M., Citil M.

REVUE DE MEDECINE VETERINAIRE, cilt.157, sa.4, ss.179-184, 2006 (SCI İndekslerine Giren Dergi) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 157 Konu: 4
  • Basım Tarihi: 2006
  • Dergi Adı: REVUE DE MEDECINE VETERINAIRE
  • Sayfa Sayıları: ss.179-184

Özet

L-carnitine is an essential cofactor in mitochondrial oxidation of fatty acids with antioxidant and protective effects against lipid peroxidation. We investigated the protective effect of L-carnitine on gentamicin nephrotoxicity and the changes of plasma and kidney total sialic acid concentrations with gentamicin treatments. Twenty four Balb/C mice were divided into 4 groups. Group 1 received subcutaneous (s.c.) isotonic saline daily for 5 days. Group 2 was daily treated with s.c. injection of 500 mg/kg L-Carnitine for 5 days, group 3 was treated with 100 mg/kg of gentamicin (s.c.) injection daily for 5 days, and group 4 with 500 mg/kg L-Carnitine (s.c.) plus 100 mg/kg (s.c.) gentamicin for 5 days. Plasma and tissue glutathione (GSH), malondialdehyde (MDA) and total sialic acid (TSA) concentrations were measured on day 5. Blood urea and creatinine as well as kidney histopathology were also evaluated to assess the nephrotoxic effect of gentamicin. Administration of L-carnitine significantly reduced the gentamicin-induced increases of MDA and TSA concentrations in the plasma and kidneys. In addition. L-carnitine reduced the gentamicin-nephrotoxicity as evidenced by blood urea, creatinine and kidney histopathology. L-carnitine also improved the antioxidant status in the plasma and kidneys of gentamicin treated mice by significantly increasing GSH concentration compared to controls and to mice treated with gentamicin alone. These results suggest that L-carnitine may attenuate gentamicin-induced nephrotoxicity by improving antioxidant status, and reducing tissular lesions in Balb/C mice.