OBJECTIVE AND DESIGN: The study was designed to elucidate whether cyclosporine A (Cy A) induces oxidative stress in heart, liver and kidney. MATERIAL AND TREATMENT: Male Wistar rats were treated with NaCl (n = 7), cremophor (vehicle for Cy A: n = 7) and 30 mg/kg b.w. Cy A in cremophor (n = 7) daily for 4 weeks. METHODS: Oxidized (GSSG) and reduced (GSH) glutathione, lipid peroxides and superoxide dismutase were measured in the organs. RESULTS: Increases in GSSG [nmol/mg prot.] and a compensatory rise in total GSH [nmol/mg prot.] indicating Cy A-induced oxidative stress were found in kidney (0.39 +/- 0.09 vs. 0.47 +/- 0.14 vs. 0.64 +/- 0.18; 20.71 +/- 3.86 vs. 21.07 +/- 3.86 vs. 28.14 +/- 3.37) and liver (0.51 +/- 0.11 vs. 0.51 +/- 0.09 vs. 0.65 +/- 0.25; 33.35 +/- 5.06 vs. 32.88 +/- 5.12 vs. 44.12 +/- 6.06) but not in heart. CONCLUSION: Cy A-induced oxidative stress may contribute to the hepatotoxicity and nephrotoxicity of this drug. After heart transplantation, accelerated allograft atherosclerosis limits transplantation success. We did not find any evidence that Cy A induces oxidative stress in the heart which might favour atherogenesis.
OBJECTIVE AND DESIGN: The study was designed to elucidate whether cyclosporine A (Cy A) induces oxidative stress in heart, liver and kidney. MATERIAL AND TREATMENT: Male Wistar rats were treated with NaCl (n = 7), cremophor (vehicle for Cy A: n = 7) and 30 mg/kg b.w. Cy A in cremophor (n = 7) daily for 4 weeks. METHODS: Oxidized (GSSG) and reduced (GSH) glutathione, lipid peroxides and superoxide dismutase were measured in the organs. RESULTS: Increases in GSSG [nmol/mg prot.] and a compensatory rise in total GSH [nmol/mg prot.] indicating Cy A-induced oxidative stress were found in kidney (0.39 +/- 0.09 vs. 0.47 +/- 0.14 vs. 0.64 +/- 0.18; 20.71 +/- 3.86 vs. 21.07 +/- 3.86 vs. 28.14 +/- 3.37) and liver (0.51 +/- 0.11 vs. 0.51 +/- 0.09 vs. 0.65 +/- 0.25; 33.35 +/- 5.06 vs. 32.88 +/- 5.12 vs. 44.12 +/- 6.06) but not in heart. CONCLUSION:Cy A-induced oxidative stress may contribute to the hepatotoxicity and nephrotoxicity of this drug. After heart transplantation, accelerated allograft atherosclerosis limits transplantation success. We did not find any evidence that Cy A induces oxidative stress in the heart which might favour atherogenesis.
Authors: Despina N Perrea; Konstantinos G Moulakakis; Maria V Poulakou; Ioannis S Vlachos; Antonios Papachristodoulou; Alkiviadis I Kostakis Journal: Int Urol Nephrol Date: 2006 Impact factor: 2.370