RENAL FAILURE, no.ISSN: 0886-022X print / 1525-6049 online DOI: I 0. I 080/08860220'7 0 139 17 38, pp.535-542, 2007 (SCI-Expanded)
Reactive oxygen species EOS) were shown to contribute to
the çellular damage induced by ischemia_reperfusion. The purpose
of this study was to investigate and compare the efficiency of melatonin and vitamin E in the reduction of injury induced by ROS in a
rat model of renal isçhemia-reperfusion. Twenty-four Wistar-albino
rats were divided into fow groups. Rats in the Sham group were
given saline I ml/kg, intraperitoneally (ip) 72h,48 h, 24h, and 30
min before the sham operation. Rats in ischemia-reperfusion (IR),
üt+Melatonin, and IR+Vitamin E groups were given saline (l mL/
kg), melatonin (10 mg&g), and vitamin E (100 mg&g) ip, respeatively, 72h,48 h, 24h, and 30 min before the isçhemia for 60 min,
followed by reperfusion for 60 min. The blood samples and kidney
tissues of the rats were taken under anesthesia. Ischemia-reperfusion significantly increased urea, creatinine, and malondialdehyde
O4DA) levels, and decreased superoxide dismutase (SOD) and catalase (CAT) activities. Histopathological findings of the IR group
confirmed that there was renal impairment by cast formation and
tubular necrosis in the tubular epithelium. In the lR+Melatonin
group, while MDA levels significantly decreased, SOD activities
inçreased. In the lR+Melatonin grouP, the level of tubular neçroşis
and çast formation are significantly decreased than those Seen in the ischemia-reperfusion group. Melatonin in particular was effective
to reverse hot ischemia of kidney by its antioxidant effects. These
results may indicate that melatonin prefreatment protects against
functional, biochemical, and morphological damage better than
vitamin E in renal ischemia-reperfusion injury.