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Drug-resistance and adverse effects of current drugs are the most obstacles in the treatment of epilepsy. In a plan for finding new natural anticonvulsant agents, we studied the anticonvulsant effects of essential oil (ZMEO) and methanolic extract (ZMME) of Zhumeria majdae in pentylene tetrazol (PTZ) and maximal electro-shock (MES) models in mice. Mice received different doses of ZMEO and ZMME, 30 min before induction of chemical and electrical convulsions. Neurotoxicity (movement toxicity and sedation) was evaluated using rota-rod test. The mortality was determined after 24 h following injection of different doses of the ZMEO and ZMME. The obtained results show that ZMEO dose-dependently protected mice from tonic convulsions induced by PTZ and MES with effective doses (ED(50)) of 0.26 (0.13-0.39) and 0.27 (0.17-0.37) ml/kg respectively. Toxic doses (TD(50)) in rota-rod test for ZMEO was 0.55 (0.42-0.70) ml/kg. ZMME at dose of 2 g/kg decreased tonic convulsions as much as 40 %. For ZMEO, TD(50) of 0.55 (0.45-0.69) ml/kg was obtained. ZMME significantly decreased the walking time in rota-rod test at dose of 2 g/kg. Lethal dose (LD(50)) of ZMEO was determined as 2.35 (1.98-2.65) ml/kg. ZMME showed about 34 % death of the animals at dose 5 g/kg. The essential oil of Z. majdae could be a good candidate for further anticonvulsive studies.

Diazinon (Dz) is a widely used insecticide. It can induce nephrotoxicity and neurotoxicity via oxidative stress. Captopril, an angiotensin-converting enzyme inhibitor, is known for its antioxidant properties. In this study, we used captopril for ameliorating of Dz-induced kidney and brain toxicity in rats. Animals were divided into five groups as follows: negative control (olive oil), Dz (150 mg kg), captopril (60 and 100 mg kg) and positive control (N-acetylcysteine 200 mg kg) were injected intraperitoneally 30 min before Dz. After 24 h, animals were anesthetized and the brain and kidney tissues were separated. Then oxidative stress factors were evaluated. Also, blood was collected for assessment of blood urea nitrogen (BUN), creatinine (Cr) and nitric oxide (NO) levels. Dz significantly increased oxidative stress markers such as reactive oxygen species (ROS), lipid peroxidation, and protein carbonyl as well as glutathione (GSH) oxidation in both tissues. Increased levels of the BUN, Cr and NO were observed after Dz injection. Interestingly, captopril administration significantly decreased ROS production in both tissues. Captopril significantly protected kidney and brain against lipid peroxidation and GSH oxidation. Administration of captopril could markedly inhibit protein carbonyl production in kidney and brain after Dz injection. Furthermore, captopril ameliorated the increased level of BUN, Cr and NO. These results suggested that captopril can prevent Dz-induced oxidative stress, nephrotoxicity and neurotoxicity because of its antioxidant activity.

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The aim of this study was to evaluate the toxic effect of AlNPs on rat brain mitochondria and compare it with that of aluminium's ionic form. METHODS: Mitochondria were isolated from rat brain. Isolated mitochondria were treated with normal saline (Control) and different concentrations of aluminium ions (AlIs) and AlNPs (50, 100 and 200 μM). Then, the effect of AlNPs on electron transport chain complexes as well as various endpoints such as mitochondrial oxidative damage (reactive oxygen species, lipid peroxidation, glutathione, and protein carbonyl) and mitochondrial function were assessed. Also, apoptosis was evaluated by cytochrome c release, mitochondrial membrane potential and swelling. RESULTS: When compared to the control group, the exposure to AlNPs showed a marked elevation in oxidative stress markers and inhibition of complex III which was accompanied by disturbance in mitochondrial function. Also, AlNPs induced a signifi cant collapse of mitochondrial membrane potential, mitochondrial swelling, and cytochrome c release. CONCLUSIONS: The comparison of mitochondrial toxicity markers between both forms of aluminium revealed that the toxic effect of AlNPs on isolated brain mitochondria was substantially greater than that that caused by AlIs, which can probably be ascribed to its higher reactivity (Tab. 1, Fig. 8, Ref. 45).

Objective: Stainless steel crowns (SSCs) are preformed metal crowns used to restore severely decayed primary teeth. The aim of this study is to evaluate the effects of pH changes and SSC margin trimming on nickel release in artificial saliva solution. Methods: A total of 90 SSCs were divided into three groups and placed in 35 ml of artificial saliva of pH 6.8, 5, and 3.5. Another group consisting 30 SSCs with trimmed margins was placed in saliva of pH 6.8. All SSCs were incubated at 37°C. The concentration of released nickel was assessed on days 1, 7, 14, 21, and 28 by atomic absorption spectrophotometry. Results: The highest concentrations of nickel were released on the first day in all groups. Nickel release increased with decreasing pH, and the differences observed were statistically significant on days 1, 7, 14, and 28. SSC trimming caused a significant increase in nickel release on all days except day 21. Conclusion: The concentration of nickel increased in saliva of low pH. The highest levels of nickel were released with SSC margin trimming because of the loss of integrity of the margins.

Ethanol is the most widely abused drug in the world and its long-term use induces oxidative stress in the liver tissue. The aim of this study was to evaluate protective effect of Viola odorata against ethanol-induced hepatotoxicity in Wistar rat. Animals were divided into 9 groups as follows: control (normal saline), ethanol (10 mg/kg, intraperitoneally), ethanol with 3 doses (125, 250, and 500 mg/kg) of ethyl acetate flower and leaf extracts, and positive control (vitamin E 80 mg/kg). Animals were gavaged 30 min before ethanol injection for 28 days. Then, animals were killed and the livers were separated. Oxidative stress parameters, including reactive oxygen species, lipid peroxidation, and protein carbonyl as well as glutathione content, were evaluated. Also, histopathological examination was performed and assessment of blood alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total antioxidant capacity were evaluated. Ethanol significantly increased oxidative stress markers in liver. Interestingly, administration of both extracts significantly decreased oxidative stress markers in liver tissue and biochemical parameters in the plasma. In addition, abnormal pathological features were improved after treatment with flower and leaf extracts. These results suggested that V. odorata can be considered a candidate for improving conditions due to ethanol-induced tissue oxidative damage because of its antioxidant activity.