Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study.

Spinal cord injury (SCI) induced oxidative stress affects multiple organ systems including the kidney. We studied the possible protective effects of melatonin on SCI-induced oxidative damage in renal tissues of rats. Wistar albino rats (n = 24) were exposed to SCI and divided into vehicle- or melatonin-treated SCI groups. Melatonin was administred intraperitoneally at a dose of 10 mg/kg for seven days. Renal tissues were investigated by light and electron microscopy. Furthermore, tissue malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were also determined. In the vehicle-treated SCI group, the renal histology was disturbed compared to controls, whereas the melatonin-treated SCI group showed significantly reduced degeneration of renal tissue as seen by both light and electron microscopy. MDA levels, MPO and SOD activities were increased and GSH levels were decreased in the vehicle-treated SCI group compared to controls. On the other hand, decreased MDA levels and MPO activities and increased GSH levels were observed in the melatonin-treated SCI group compared to vehicle-treated SCI group. These results showed that experimentally induced SCI caused oxidative stress in the rat kidney, whereas melatonin treatment reduced oxidative stress, suggesting that it may be used as a complementary therapy of renal problems occurring following SCI.

The effects of Nigella sativa against oxidative injury in a rat model of subarachnoid hemorrhage.

OBJECTIVE: The aim of the study was to investigate the putative neuroprotective effect of Nigella sativa oil (NSO) treatment against subarachnoid hemorrhage (SAH) in rats. METHODS: To induce SAH, rats were injected with 0.3 ml blood into their cisterna magna. Male Wistar albino rats were divided as control, vehicle-treated SAH, and NSO-treated (0.2 ml/kg, intraperitoneally) SAH groups. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for blood brain barrier permeability, brain water content, or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na(+)-K(+)-ATPase activities. RESULTS AND DISCUSSION: On the second day of SAH induction, neurological examination scores were increased in SAH groups, while SAH caused significant decreases in brain GSH content and Na(+)-K(+)-ATPase activity, which were accompanied with significant increases in MDA levels and MPO activity. The histological observation showed vasospasm of the basillary artery. On the other hand, NSO treatment markedly improved the neurological scores while all oxidant responses were prevented, implicating that NSO treatment may be of therapeutic use in preventing oxidative stress due to SAH.