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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.

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).

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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.

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.

Background:Cadmium is a heavy metal that can cause various injuries in the body, including nephrotoxicity. L-Arginine is a metal chelator that can prevent oxidative damage caused by oxygen free radicals. Objectives:This study aimed to investigate the effect of L-arginine in inhibiting mitochondrial toxicity induced by subchronic cadmium exposure in the kidney of male mice. Methods: A total of 42 male mice were randomly divided into six groups (n=6): control (normal saline), cadmium (2 mg/kg), cadmium (2 mg/kg) plus three doses of L-arginine (50, 100, and 200 mg/kg) and finally cadmium (2 mg/kg) plus vitamin C (500 mg/kg). After 42 days, the animals were anesthetized with ketamine/xylazine. Their kidney tissues were removed, and mitochondrial fractions were isolated. Oxidative stress factors and mitochondrial damage parameters (MTT, swelling, and mitochondrial membrane potential) were measured in renal isolated mitochondria. Also, evaluation of Blood Urea Nitrogen (BUN) and Creatinine (Cr) tests were done. Results: Significant rise in BUN and Cr were observed in cadmium-treated mice (P<0.05). Cadmium enhanced oxidative stress in the kidney via increasing lipid peroxidation and oxidation of protein and glutathione. It caused significant mitochondrial dysfunction, mitochondrial membrane potential collapse, and swelling in isolated mitochondria (P<0.05). L-Arginine significantly ameliorated cadmium-induced oxidative stress and mitochondrial damage (P<0.05). Furthermore, a significant reduction in serum BUN and Cr were observed in L-arginine received group (P<0.05). Conclusion: The results showed that L-arginine has significant protective effects against cadmium-induced renal toxicity in male mice.