Reactive oxygen species (ROS) were shown to contribute to the cellular 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
ischemia-reperfusion. Twenty-four Wistar-albino rats were divided into four groups. Rats in the
Sham group were given saline 1 mL/kg, intraperitoneally (ip) 72 h, 48 h, 24 h, and 30 min before the
sham operation. Rats in
ischemia-reperfusion (IR), IR+Melatonin, and IR+Vitamin E groups were given saline (1 mL/kg),
melatonin (10 mg/kg), and
vitamin E (100 mg/kg) ip, respectively, 72 h, 48 h, 24 h, and 30 min before the
ischemia 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 (MDA) 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 IR+Melatonin group, while MDA levels significantly decreased, SOD activities increased. In the IR+Melatonin group, the level of tubular
necrosis and cast 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 pretreatment protects against functional, biochemical, and morphological damage better than
vitamin E in renal
ischemia-reperfusion injury.