Alzheimer's disease is a progressive neurodegenerative disorder with decline in memory. The role of oxidative stress is well known in the pathogenesis of the disease. The purpose of this study was to evaluate pretreatment effects of oleuropein on oxidative status and cognitive dysfunction induced by colchicine in the hippocampal CA1 area. Male Wistar rats were pretreated orally once daily for 10 days with oleuropein at doses of 10, 15 and 20 mg/kg. Thereafter, colchicine (15 μg/rat) was administered into the CA1 area of the hippocampus to induce cognitive dysfunction. The Morris water maze was used to assess learning and memory. Biochemical parameters such as glutathione peroxidase and catalase activities, nitric oxide and malondialdehyde concentrations were measured to evaluate the antioxidant status in the rat hippocampus. Our results indicated that colchicine significantly impaired spatial memory and induced oxidative stress; in contrast, oleuropein pretreatment significantly improved learning and memory retention, and attenuated the oxidative damage. The results clearly indicate that oleuropein has neuroprotective effects against colchicine-induced cognitive dysfunction and oxidative damage in rats.

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Protozoa aggregate to or avoid from chemical substances. We aimed to show the significance of nitric oxide (NO) in the performance of the eukaryotes to misuse drug exposure. The micro-organism Paramecium caudatum was collected from natural sources and properly isolated by repeatedly sub-cultivation in hay infusion. Number of cells per 1ml of pure medium culture was counted using Sedgwick-Rafter cell chamber. Doses of naloxone (0.05-0.4µg/µl) solely or jointly with the NO agents were infused into the chamber. Cell response was recorded after drug infusion with intervals (0-180 sec). Negative control received distilled water (1µl) instead of naloxone (legend 0). Along with, the Ca channels or cGMP pathway was banded to discuss the mechanism. According to the results, the Paramecia showed negative chemo-taxis to the naloxone, the response which is comparable with signs of withdrawal from abused drugs. This response was potentiated by activation of NO system, but, reversed after usage of the system blocker. The inhibition of Ca channels or cGMP signaling pathway markedly enhanced the avoidance. In conclusion, this study may clearly contribute the signal molecule NO in the dependence of the eukaryotes on sedative misuse drugs.