Pharmacological studies allow to suggest that activation of cannabinoid type 1 receptors (CB1) have a neuroprotective role against toxicity induced by organophosphate agents, but the exact mechanisms of this effect as well as interaction with receptors of other types are far from clear. Therefore, the aim of current study was to evaluate the effect of CB1 and NMDA receptors agonists on cell viability and biomarkers of oxidative stress and lipid peroxidation in PC12 cells exposed to paraoxon. PC12 cells were exposed to 100 µm paraoxon as organophosphate agent. Treatments with 1 µm arachidonyl-2'-chloroethylamide (aCea) as specific agonist of CB1 receptors, 100 µM N-methyl-D-aspartate (NMDA) as agonist of NMDA receptors and 1 µm am251 as antagonist of CB1 receptors were done. Cell via bility and biomarkers of oxidative stress were evaluated after 48 h of incubation. The level of CB1 receptor protein was evaluated by Western blotting. It was demonstrated that PC12 cells treatment with paraoxon led to cell viability inhibition, glutathione level, superoxide dismutase and catalase activity reduction, lipid peroxidation intensification and CB1 receptor expression attenuation. application of aCea and Nmda was shown to be followed by normalization of these indices. The protective effect of ACEA was abolished when the CB1 receptors antagonist AM251 was applied. The study revealed that application of aCea and Nmda can protect PC12 cells against paraoxon induced toxicity through antioxidant capacity increment, lipid peroxidation inhibition and enhanced expression of CB1 receptors. K e y w o r d s: CB1 receptors, cannabinoid, paraoxon , PC12 cells, oxidative stress.

Objectives:The aim of the present study was to determine the rate, risk factors and genotypes of Hepatitis B virus amongst imprisoned men as a high-risk subpopulation. Patients and Methods:This study was an anonymous cross-sectional study conducted on 3000 sentenced men in Karaj jails from 1 December 2008 to 28 November 2009. HBV serological markers [hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg)], human immunodeficiency virus antibody (anti-HIV) and hepatitis C antibody (anti-HCV) were analyzed by the ELISA technique. Nested PCR was done for the detection of HBV DNA and patterns of restriction fragment length polymorphisms (RFLP) were obtained to determine the HBV genotypes. These patterns were confirmed by direct sequencing. Results: Hepatitis B surface antigen (HBsAg) was found in 122/3000 (4.1%) prisoners. Hepatitis B e antigen (HBeAg), anti-HIV, anti-HCV and anti-HIV/anti-HCV were detected in 52/122 (42.6%), 12/122 (10%), 22/122 (18%) and 3/122 (2.4%) prisoners, respectively. The HBV-DNA was found in 115/122 (94.3%) prisoners. The most high risk behavior was to utilize the collaborative syringe by injecting drug users (IDUs) with or without other risk factors (75.3%). Genotype D1 was obviously the only predominant type (100%). Conclusions:The rate of HBV in prisoners was significantly higher than that reported for the general population (4.1% vs. < 2%). Blood borne viral co-infections were prevalent in HBsAg positive prisoners. Continual tracing of genotypes and risk factors are helpful for identifying transmission patterns and target at-risk groups for preventive programs. High rates of HBV in prisoners indicates the need for extensive free of charge vaccination of this subpopulation.Hepatitis B is the most serious type of viral hepatitis infection. It can cause chronic liver disease and puts people at a high risk of death from cirrhosis of the liver and liver cancer. Worldwide, about two billion people have been infected with the hepatitis B virus (HBV) and more than 240 million have chronic (long-term) liver infections. About 600,000 people die every year from this serious infection. Unfortunately, high rate of intravenous drug use, high-risk sexual behaviors and overcrowding have increasingly made prisons a breeding ground for hepatitis B infection.

It is well known that production of ROS compounds and generation of oxidative stress during diabetes are the most important mechanisms of tissue damage. The aim of this study was to examine the effects of atorvastatin treatment, as an antioxidant, to prevent the brain tissue oxidative stress in streptozotocin-induced diabetic rats. Male Wistar rats were randomly divided into four groups (five rats in each group) as followed: normal, normal treated was orally received 20 mg/kg/day atorvastatin for 30 days, diabetic group was given 40 mg/kg streptozotocin by intravenous injection and diabetic treated similar to normal treated rats. After 30 days of treatment, rats were sacrificed under deep anesthesia to remove the brain. After tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods. In addition to increase blood glucose level in diabetic rats (78%), brain SOD and CAT activities were significantly increased compared with normal rats. Also, diabetes significantly decreased the GSH content of brain tissue by 57%, and increased the brain MDA level by 35%. Finally treatment with atorvastatin significantly decreased the augmented brain CAT activity and the MDA level during diabetes. Based on the finding of this study, diabetes-induced hyperglycemia provoked the production of free radicals in the brain tissue that leading to oxidative stress. Also, treatment with atorvastatin may have prevented from hyperglycemia-induced oxidative stress in the brain of diabetic rat.

It has been demonstrated that peroxisome-proliferator activated receptor-alpha (PPARα) has a potent neuroprotective role in various pathological events of the nervous tissue. Since oxidative damage is associated with development of seizure, we aimed to examine whether the PPARα agonist, fenofibrate, exerts protective effects against the repeated seizures in pentylenetetrazol (PTZ) kindling model in mice through improving the brain antioxidant capacity. The experiment was carried out in two groups of mice (each group, n = 12): PTZ-kindled mice and fenofibrate-treated kindled mice. Repetitive intraperitoneal injections of PTZ (65 mg/kg) once every 48 h were used to achieve the kindling seizures till day 21. The mice were administered orally fenofibrate (30 mg/kg/day) during the test. Latency and the brain activities of catalase and superoxide dismutase (SOD) as well as the brain content of reduced glutathione (GSH) were determined at termination of the experiment. The latency following the last injection of PTZ was considerably decreased in untreated kindled mice (49 ± 8 s), whereas fenofibrate treatment prevented this reduction in kindled mice (105 ± 16 s). Treatment with fenofibrate significantly increased the GSH content in kindled mice (20.22 ± 9.87 nmol/mg protein) compared to untreated kindled mice (5.37 ± 0.84 nmol/mg protein), (p < 0.05). Likewise, treatment with fenofibrate considerably increased the activities of catalase and SOD in kindled mice compared to untreated kindled mice by 78% and 55%, respectively. In view of the critical protective role of antioxidants in seizures, the findings of the present study suggested that the PPARα agonist, fenofibrate, might modulate the seizure behaviors in the PTZ kindling model in mice through improving the brain antioxidant capacity.