Background Cyclosporine (CsA) causes a dose-related decrease in renal funct
ion in experimental animals. Different mediators for CsA nephrotoxicity hav
e been suggested; oxygen free radicals are one of them. In experimental mod
el of Wistar rats, the roll? of antioxidant melatonin (Mel), the main produ
ct of pineal secretion, was investigated in CsA nephrotoxicity,
Methods, Male Wister rats were divided into four groups: saline control, 50
mg/kg CsA, 500 mu g/kg Mel, and CsA + Mel. At the end of 14th day of treat
ment, blood urea, creatinine, malondialdehyde, and creatinine and lithium c
learance were estimated, Histopathological examination of kidney from all t
he groups was performed.
Results. CsA caused marked elevation in blood urea, serum creatinine, and p
lasma malondialdehyde and a decrease in creatinine and lithium clearance. M
el significantly antagonized CsA-induced renal impairment. Microcalcificati
on in corticomedullary junction seen with CsA was prevented by Mel.
Conclusion. These results indicate that Mel, through its antioxidant proper
ties, provides protection against CsA-induced nephrotoxicity.