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    The protective effect of melatonin on adriamycin-induced acute cardiac injury
    (Elsevier Science Inc, 2003) Koçak, G; Erbil, KM; Özdemir, I; Aydemir, S; Sunar, B; Tuncel, M; Atalay, S
    BACKGROUND: Cardiotoxicity is the main complication of adriamycin (ADR), which is a widely used chemotherapeutic agent. OBJECTIVE: To examine the potential cardioprotective effect of melatonin (MEL) on acute ADR cardiotoxicity in a rat model. METHODS: Cardioprotection was assessed on the basis of myocardial lipid peroxidation and ultrastructure. Rats were given MEL at a daily dose of 5 mg/kg and ADR 15 mg/kg, intraperitoneally. The MEL-1 group rats received one dose and the MEL-7 group rats six daily doses of MEL and were sacrificed at the end of one and seven days, respectively. Rats in the ADR-1 and ADR-7 groups were each given a single dose of ADR, and were then sacrificed 24 h and seven days later, respectively. The MEL+ADR-1 group rats received one dose each of ADR and MEL simultaneously and were sacrificed 24 h later. The MEL+ADR-7 group received a single dose of ADR plus a daily MEL dose for six consecutive days, and were sacrificed seven days after the ADR injection. RESULTS: Lipid peroxidation products were elevated in both ADR-1 and ADR-7 groups, and this elevation was significantly inhibited by MEL treatment. Electron microscopy confirmed that ADR was positively cardiotoxic after one and seven days of exposure. The extent of ADR-induced myocardial damage was markedly reduced when MEL was combined with ADR (MEL+ADR-1 and MEL+ADR-7). CONCLUSION: The results suggest that MEL is highly efficacious at reducing the acute cardiotoxic effects of high dose ADR, and that it acts by preventing lipid peroxidation.
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    Protective effect of melatonin on experimental spinal cord ischemia
    (Springernature, 2003) Erten, SF; Kocak, A; Ozdemir, I; Aydemir, S; Colak, A; Reeder, BS
    Study design: Experimental animal model to assess ischemic spinal cord injury following occlusion of the thoraco-abdominal aorta. Objectives: To measure whether melatonin administered to rabbits before and after occlusion exerts an effect on the repair of ischemia-reperfusion (IR) injury. Setting: Medical Biology Laboratory, Inonu University, Malatya, Turkey. Methods: Rabbits were divided into three IR treatment groups and one sham-operated (ShOp) control group. The three treatment groups had their infrarenal aorta temporarily occluded for 25 min, while the ShOp group had laparotomy without aortic occlusion. Melatonin was administered either 10 min before aortic occlusion or 10 min after the clamp was removed. Physiologic saline was administered to the control animals. After treatment, the animals were euthanized and lumbosacral spinal cord tissue was removed for the determination of relevant enzyme activities. Results: Malondialdehyde levels, indicating the extent of lipid peroxidation, were found to be significantly increased in the nonmelatonin treated (IR) group when compared to the ShOp group. Melatonin, whether given to pre- or post occlusion groups, suppressed malondialdehyde levels below that of the ShOp group. Catalase (CAT) and glutathione peroxidase (GSH-Px) enzyme activities were increased in the IR group compared to the ShOp group. Melatonin given preocclusion resulted in a significant decrease in both CAT and GSH-Px enzyme levels. The superoxide dismutase ( SOD) enzyme activity was decreased in the ischemia-reperfusion treatment group. However, the melatonin treatment increased SOD enzyme activity to levels approximating that of the ShOp group. Conclusion: To our knowledge, this is the first study that shows the effects of melatonin administered both pre- and postischemia on induced oxidative damage to injured spinal cords. Our data also expands on reports that melatonin administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.