mojtaba keshavarz

Habitat assessment is the most important step in environmental decisions. One of the ways to assess habitat quality is to use habitat suitability for fish species. So, this study was conducted in Klarood River, one of the important tributaries of Babolrood River in Mazandaran Province, north of Iran to evaluate the habitat quality for Capoeta razii. At first, a site with the least anthropogenic influences was selected on the river. Then the fish was caught by electrofishing device aggregate at 100 points. At each point where the fish was caught, environmental parameters such as depth, water velocity, type of biotic and abiotic substrate were also measured. The results showed that the species prefers water velocity of 16-30 cm s-1 and depth of 16-115 cm. Moreover, suitable abiotic and biotic substrates were Macrolithal, Mesolithal and Microlithal" as well as LPTP (Live parts of terrestrial plants) respectively. Generally, the results of this study showed the appropriate function of the model in assessing the habitat suitability of this species and it can be used as a guide for quantitative assessment of habitat as well as recognizing the behavioral characteristics of the studied species.

Universal Design (UD) means designing the products and environments everyone can use as far as possible without requiring specialized compatibility or design. The present study aimed to design and develop a comprehensive and valid checklist to evaluate the design of banks based on UD principles and implement it in Iranian banks.

Based on the seven UD principles and using a mixed methods sequential exploratory design, an initial checklist with 61 items was developed. Then, its psychometric properties were evaluated based on face and content validity and inter-rater agreement. The final checklist was prepared based on the results of this stage and used in the next stage to evaluate the design of 17 banks.

The final checklist consisted of 10 areas (as per the seven UD principles). The Content Validity Ratio (CVR) and Content Validity Index (CVI) were calculated as 0.91 and 0.93, respectively. Based on areas of the checklist, all the evaluated banks showed many problems, the most significant of which were related to the areas of equal use by different groups, flexibility in use, and the size and space of access and use.

The present study’s findings led to the design of a comprehensive and standard checklist to evaluate the design of banks in terms of UD principles. The results indicated that the UD principles were not observed in most studied banks, and they need to implement targeted design interventions.

Neuroinflammation was indicated in the pathophysiology of Alzheimer’s disease(AD). Previous reports have also signified that spironolactone has anti-inflammatory effects.Therefore, the aim of this study was to assess the modulatory effects of spironolactone onneuroinflammation and memory loss in a rat model of AD.

The β-amyloid protein fragment 25-35 (Aβ) was injected in the dorsal hippocampus (5μg/2.5 μL each side) of male Sprague-Dawley rats for four consecutive days to induce memoryimpairment. Animals have intraperitoneally received spironolactone (10, 25, or 50 mg/kg, N = 6/group) or vehicle for 14 days. The passive inhibitory avoidance and the novel recognition testswere used for memory evaluation. Neuroinflammation was assessed by measuring the level ofIba1 protein, a marker of microglial activation, using western immunoblotting.

Different doses of spironolactone showed no significant changes in latency times anddiscriminations ratios in passive inhibitory avoidance and novel recognition tests, respectively,as compared to vehicle. However, spironolactone-treated groups showed significantly lowerIba1 protein levels in comparison to the vehicle-treated group (P < 0.01).

Spironolactone had a modulatory effect on neuroinflammation through a repressiveeffect on microglial activation with no valuable effect on memory improvement in a rat modelof AD. The findings of this study suggest that Aβ-induced memory loss may not be directly linkedto microglial activation. Spironolactone may be a potential candidate to be examined in otherneuroinflammatory disorders.

This survey was done in order to use of different levels of the herbal supplement Digestrum P. A. P. in freshwater Angel fish (Pterophyllum scalare) fry and its effect on some growth performance; microbial Flore and morphology of the intestine. 120 fries (1.2±0.4gr) were gathered in a Complete Randomize Design plan with 4 treatments fed on different levels of Digestrum (0, 1, 1.5 and 2 gr/kg in dried food) each with 3 replicates for 60 days. The results showed that Digestrum had positive effects on final body weight, SGR and FCR so that in the treatment fed on 2 gr/kg. The most final weight (6.8g±0.34), the best SGR (4.0±0.12) and the least FCR (1.1±0.22) were observed in the same treatment (p<0.05). The most number of Lactobacilli colonies, the best length of the intestinal villies (600.14±15.44), villi across (105.14±2.18), and cript depth (55.2±2.10) were reported from this treatment too (p<0.05). Based on the results, it could be concluded that the herbal supplement Digestrum P. A. P. can improve growth performance and intestinal bacterial flore in 2gr/kg level of dried diet.

Spironolactone has produced beneficial effects in animal models of neurodegenerative disorders. However, the underlying mechanisms of this agent on neurons and glia are mostly unknown. Therefore, we aimed to show the effects of spironolactone and fludrocortisone, a mineralocorticosteroid receptor agonist, on neuronal and glial toxicity induced by N-methyl-D-aspartate (NMDA) activation and chloroquine, an autophagy inhibitor, in the cell culture. We exposed the SHSY5Y neuroblastoma and 1321N1 astrocytoma exposed to NMDA (25µM), or chloroquine (40µM) for 24 and 48h to induce neuronal and glial toxicity. Spironolactone (1, 10, and 20µM) or fludrocortisone (300nM) were also added to the cells for 24 and 48h. Cell survival was measured using the MTT assay. Neurons and astrocytes treated with NMDA and spironolactone (1, 10, and 20µM) for 24 and 48h had lower cell death compared with the NMDA-treated group. Moreover, cells treated with NMDA and fludrocortisone for 24 and 48h had higher viability in comparison to the NMDA-treated group. The neuronal cells treated with chloroquine and spironolactone (10 and 20µM) for 24h had higher cell viability compared with the chloroquine group. Chloroquine plus spironolactone (20µM) treatment for 24 and 48h increased cell viability of astrocytes compared with the chloroquine-treated group. Moreover, the treatment of neurons and astrocytes with chloroquine plus fludrocortisone for 24h decreased cell death.  Spironolactone and fludrocortisone protected neurons and astrocytes against NMDA- and chloroquine-induced toxicity. The mechanism of neuronal and glial protective effects of spironolactone possibly related to the inhibition of the mineralocorticosteroids. However, spironolactone might affect other non-mineralocorticoid systems.

Glycogen synthase kinase (GSK)-3β mediates amyloid-beta (Aβ) and oxidative stress-induced neurotoxicity in neurodegenerative disorders. Natural products with antioxidant activity, such as Sargassum (S.) oligocystum may modulate GSK-3β enzyme and protect against Aβ-induced neurotoxicity. Therefore, we aimed to assess the neuroprotective effects of a methanolic extract of S. oligocystum against Aβ-induced neurotoxicity in the SH-SY5Y cells and the contribution of GSK-3β inhibition to the neuroprotective effects of the S. oligocystum extract. SH-SY5Y neuroblastoma cells were seeded in 96 well plates and incubated with Aβ (20µM) and the methanolic extract of S. oligocystum (40, 50, and 70μg/ml) for 24h. We measured cell viability using the MTT assay. Western blot method was used to measure the expression of the GSK-3β and phosphorylated (p)-GSK-3β protein levels. The data were analyzed using one-way analysis of variance (ANOVA) followed by the LSD test. Amyloid-beta (20µM) reduced neuronal cell viability compared with the control group. Addition of S. oligocystum extract at concentrations of 40, 50 and 70μg/ml decreased the neurotoxic effects of Aβ. The extract of S. oligocystum at a concentration of 70μg/ml also decreased the effects of Aβ on the GSK-3β protein level. The pGSK-3β protein levels in the S. oligocystum groups (40 and 70μg/ml) plus Aβ were lower than the Aβ-treated group. The methanolic extract of S. oligocystum protected SH-SY5Y cells from Aβ-induced neurotoxicity. The attenuation of the GSK-3β protein level may contribute to the neuroprotective effects of S. oligocystum extract.

Spironolactone has produced beneficial effects in animal models of neurodegenerative disorders. However, the underlying mechanisms of this agent on neurons and glia are mostly unknown. Therefore, we aimed to show the effects of spironolactone and fludrocortisone, a mineralocorticosteroid receptor agonist, on neuronal and glial toxicity induced by N-methyl-D-aspartate (NMDA) activation and chloroquine, an autophagy inhibitor, in the cell culture. We exposed the SHSY5Y neuroblastoma and 1321N1 astrocytoma exposed to NMDA (25µM), or chloroquine (40µM) for 24 and 48h to induce neuronal and glial toxicity. Spironolactone (1, 10, and 20µM) or fludrocortisone (300nM) were also added to the cells for 24 and 48h. Cell survival was measured using the MTT assay. Neurons and astrocytes treated with NMDA and spironolactone (1, 10, and 20µM) for 24 and 48h had lower cell death compared with the NMDA-treated group. Moreover, cells treated with NMDA and fludrocortisone for 24 and 48h had higher viability in comparison to the NMDA-treated group. The neuronal cells treated with chloroquine and spironolactone (10 and 20µM) for 24h had higher cell viability compared with the chloroquine group. Chloroquine plus spironolactone (20µM) treatment for 24 and 48h increased cell viability of astrocytes compared with the chloroquine-treated group. Moreover, the treatment of neurons and astrocytes with chloroquine plus fludrocortisone for 24h decreased cell death. Spironolactone and fludrocortisone protected neurons and astrocytes against NMDA- and chloroquine-induced toxicity. The mechanism of neuronal and glial protective effects of spironolactone possibly related to the inhibition of the mineralocorticosteroids. However, spironolactone might affect other non-mineralocorticoid systems.

Memantine is an approved drug for the treatment of Alzheimer’s disease (AD). Autophagy, lysosome dysfunction, and sigma receptors have possible roles in the pathophysiology of AD. Therefore, we aimed to investigate the contribution of sigma receptors and lysosome inhibition to the neuroprotective effects of memantine against amyloid-beta (Aβ)-induced neurotoxicity in SH-SY5Y cells.

We determined the neuroprotective effects of memantine (2.5 µM), dizocilpine (MK801, as a selective N-methyl-D-aspartate (NMDA) receptor antagonist) (5 μM) against Aβ25– 35 (2 μg/μL)-induced neurotoxicity. We used chloroquine (10, 20, and 40 μM) as a lysosome inhibitor and BD-1063 (1, 10, and 30 μM) as a selective sigma receptor antagonist. The MTT assay was used to measure the neurotoxicity in the SH-SY5Y cells. Data were analyzed using the one-way ANOVA.

Memantine (2.5 µM), dizocilpine (5 µM), chloroquine (10 and 20 µM) and BD-1063 (1, 10 and 30 µM) decreased the neurotoxic effects of Aβ on the SH-SY5Y cells. However, chloroquine (40 µM) increased the neurotoxic effects of Aβ. Cell viability in the cells treated with memantine + Aβ + chloroquine (10, 20, and 40 μM) was significantly lower than the memantine + Aβ-treated group. Moreover, cell viability in the memantine + Aβ group was higher than the memantine + Aβ + BD-1063 (10 and 30 μM) groups.

The lysosomal and sigma receptors may contribute to the neuroprotective mechanism of memantine and other NMDA receptor antagonists. Moreover, the restoration of lysosomes function and the modulation of sigma receptors are potential targets in the treatment of AD.

Astrocyte, S100B and nitric oxide may have a role in the pathogenesis and treatment of epilepsy. However, the effects of nitric oxide and S100B on the gliotoxic effects of chemical convulsants such as pentylenetetrazole (PTZ) is unknown. Therefore, we aimed to evaluate the effects of S100B and nitric oxide on gliotoxicity of PTZ in a 1321NI1 astrocytic culture.

The 1321N1 astrocytes were exposed to PTZ (40mM), arundic acid (50μM) or both of them for 24h. In addition, we poured L-arginine (100 or 500μM), N-nitro-L-arginine methyl ester (100 or 500μM), 7-nitroindazole (30 or 100μM) and aminoguanidine (50 or 100μM) to the culture media contained PTZ, arundic acid or both of them and incubated for 24h. Cell viability was measured by the methylthiazolyldiphenyl-tetrazolium bromide reagent and the S100B protein level was measured using an enzyme-linked immunosorbent assay.

There was a negative correlation between cell viability in astrocytes and the intracellular S100B levels. PTZ decreased cell viability, but it increased the intracellular S100B levels. Arundic acid, N-nitroarginine methyl ester, 7-nitroindazole and aminoguanidine reversed the PTZ effects on cell viability and intracellular S100B levels. Adding the L-arginine to PTZ plus arundic acid reduced the modulatory effects of arundic acid on PTZ.

Nitric oxide and S100B have a role in gliotoxicity of PTZ in cell culture. Arundic acid suppresses PTZ-induced S100B elevation and gliotoxicity possibly by modulation of the nitric oxide pathway.

The reduction of glycogen synthase kinase-3β protein level may correlate to the neuroprotective effects of antioxidant agents like caffeine. Therefore, we aimed to evaluate the impact of GSK-3β protein on neuroprotective effects of caffeine in the SHSY5Y cells exposed to beta-amyloid.

We incubated SHSY5Ycells with beta-amyloid 25–35 and caffeine (0.6 and 1mM) for 24h. Cell viability was determined using MTT test. We used the western blotting technique to measure the glycogen synthase kinase-3β and phosphorylated glycogen synthase kinase-3β protein levels.

Caffeine (0.6 and 1mM) diminished beta-amyloid neurotoxicity and attenuated the beta-amyloid effects on the glycogen synthase kinase-3β protein level in a neuronal culture.

Caffeine neuroprotective effects against beta-amyloid may correlate to glycogen synthase kinase-3β protein.</div>

It has been shown that glial activation has important role in the pathophysiology of Alzheimer’s disease. S100B is an astrocyte specific factor with deleterious effects on the neuronal and non-neuronal cells in the central nervous system. Arundic acid is an agent that inhibits the secretion and production of S100B in astrocytes. Therefore, we aimed to evaluate the contribution of S100B in the cyto-protective effects of Arundic acid against beta-amyloid in 1321N1 astrocyte cell culture.

Human astrocyte cells (1321N1) were treated with beta-amyloid (200 μM) and / or Arundic acid (50 μM) for 24 hours. Cell viability was measured using the MTT (3, 4, 5-dimethylthiazole-2, 5-diphenyl tetrazolium bromide) method. The S100B protein level was measured by the ELISA method.

Beta-amyloid treatment reduced cell survival compared to the control-treated groups. In contrast, the addition of Arundic acid to beta-amyloid suppressed the beta-amyloid-induced cell death. Beta-amyloid also increased the S100B protein level. However, Arundic acid prevented the rise of S100B protein level induced by beta-amyloid.

The reduction of S100B protein secretion may be involved in the protective effects of Arundic acid against the beta-amyloid induced Glio-toxicity in the astrocyte culture.

Valproic and arundic acids are astrocytes-modulating agents with potential effects in the treatment of Alzheimer’s disease (AD). S100B is an astrocytic cytokine with a possible role in the pathogenesis of AD. In this study, we aimed to assess the glioprotective effects of valproic and arundic acids against amyloid-β-peptide (Aβ)-induced glial death and contribution of S100B to the glioprotective effects of these agents in an astrocytic culture.    We used Aβ25–35 at a concentration of 200 μM in 1321N1 astrocyte cells. We treated the cells with valproic acid (0.5 and 1 mM) and/or arundic acid 50 µM for 24 hr. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) test was used to measure cell viability. The intracellular and extracellular S100B levels were measured using an ELISA kit. The data were analyzed using one-way analysis of variance followed by the Tukey’s test.    Aβ (200 µM) decreased the cell viability compared to the control group (P<0.001). Valproic acid (0.5 and 1 mM) and arundic acid (50 µM) ameliorated the gliotoxic effects of Aβ (P<0.05). The Aβ-treated group had higher S100B levels (both intracellular and extracellular) compared to the negative control groups (P<0.001). Arundic and valproic acids (0.5 and 1 mM) decreased both the intracellular and extracellular S100B levels compared to the Aβ-treated group (P<0.001). By considering homeostatic and neuroprotective functions of astrocyte, the astroprotective effects and the attenuation of S100B level may be responsible, at least in part, for the beneficial effects of valproic and arundic acids in AD.

Cinnamaldehyde may be responsible for some health benefits of cinnamon such as its neuroprotective effects. We aimed to investigate the cinnamaldehyde neuroprotective effects against amyloid beta (Aβ) in neuronal SHSY5Y cells and evaluate the contribution of N-methyl-D-aspartate (NMDA), ryanodine, and adenosine receptors and glycogen synthase kinase (GSK)-3β, to its neuroprotective effects. After seeding the cells in 96-well plates, adenosine (20, 40, 80, and 120 µM), NMDA (20, 40, 80, and 120 µM), and dantrolene (as a ryanodine receptor antagonist; 2, 4, 6, 8, and 16 µM) were added to the medium containing Aβ25-35 and/or cinnamaldehyde. The 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide method was used to assess neurotoxicity and western blot to measure the GSK-3β protein level. Cinnamaldehyde (15, 20, 23, and 25 μM) significantly reversed Aβ-induced toxicity in SHSY5Y neuronal cells. Adenosine (20, 40, 80 and 120 μM) inhibited the neuroprotective effects of cinnamaldehyde (15 μM). NMDA (20, 40, 80, and 120 μM) reduced cinnamaldehyde (15 and 23 μM) neuroprotective effects against Aβ neurotoxicity. Dantrolene (2, 4, 8, and 16 μM) significantly reduced cinnamaldehyde (15 μM) neuroprotective effects. Cinnamaldehyde (15 and 23 μM) suppressed the Aβ-induced increment of GSK-3β protein level.  NMDA and adenosine receptors suppression together with ryanodine receptors stimulation may be relevant to cinnamaldehyde neuroprotective effects against Aβ neurotoxicity. Moreover, the inhibition of GSK-3β may contribute to the cinnamaldehyde neuroprotection.

Studies have shown that performance-enhancing drugs (PEDs) especially anabolic steroids cause liver damage. There is no study on the PEDs effects on the liver of bodybuilding athletes in Bushehr city (Iran).  Aim of this study was to evaluate the hepatic effects of PEDs, particularly anabolic steroids in male bodybuilders in Bushehr.

Demographic information, exercise program, use of PEDs, alcohol and dietary supplements were recorded in male bodybuilders using a questionnaire. Participants were divided into three groups: 1) current users (CU), 2) non-current users (NCU), and 3) non-users (NU). The serum levels of alanine transaminase (ALT), aspartate transaminase (AST) and bilirubin were measured in the athletes by using the commercially available kits. The data were analyzed by using one-way analysis of variance.

Two-hundred and three bodybuilders with the age range of 18-50 years, body mass index of 18.6-40 kg/m2, and average of 6 years exercise were included in the study. In the present study, 8.9% of athletes were current users, 39.9% were non-current users, and 51.2% were non-users. Athletes have been used anabolic steroids, stimulants, growth hormone, and insulin. The average period of PEDs use in athletes was 60 days/year by simultaneous oral and injection routes. The serum levels of ALT (p = 0.003), AST (p = 0.000) and bilirubin (p = 0.023) were significantly different between the three groups. The serum levels of ALT (p = 0.000) and AST in current users were higher than non-user athletes, while only the AST level in non-current users was higher than non-users (p = 0.044).

The use of anabolic steroids with other PEDs may raise the serum level of hepatic enzymes in male bodybuilders. This effect may be the sign of PEDs-induced hepatic injury in these athletes.

Sigma receptors, N-methyl-D-aspartate (NMDA) antagonist, and modulators of intracellular calcium may be useful for seizure control. Therefore, we aimed to evaluate the antiepileptic effects of opipramol, a sigma receptor agonist, against pentylenetetrazole (PTZ)-induced seizures in mice and assess ketamine and caffeine interaction with the antiepileptic effects of opipramol.
PTZ (100 mg/kg) was used for the induction of seizure in 72 male albino Swiss strain of mice (n=8). Opipramole (10, 20, and 50 mg/kg), ketamine (50 mg/kg), caffeine (200 mg/kg), opipramole (20 mg/kg) plus ketamine (50 mg/kg), opipramole (20 mg/kg) plus caffeine (200 mg/kg), diazepam (5 mg/kg as a positive control), and the vehicle were administered interaperitoneally 30 minutes before the injection of PTZ. The latency was recorded for the clonic, tonic-clonic seizures, and death of animals after the injection of PTZ. Kruskal-Wallis test followed by Dunn’s test was used for the analysis of data. Statistical analysis was performed with the SPSS software version 23.0 and P Opipramol (20 mg/kg) increased the latency for the PTZ-induced clonic (44%, P=0.021) and tonic-clonic (130.80%, P=0.043) seizures compared with the vehicle-treated group. Animals treated with opipramol (20 mg/kg) plus caffeine (200 mg/kg) had a significantly higher onset of PTZ-induced clonic and tonic-clonic seizures compared with the control (P=0.046 and Opipramol attenuated the seizures induced by the PTZ. Ketamine and caffeine had no effect on the anticonvulsant activity of opipramol.

Diabetes is a metabolic syndrome which is associated with the worldwide major public health problems. There are many natural compounds from the sea-market, as a valuable aquatic source, along with the variety of health and therapeutic benefits. In the present research, with respect to the traditional and ethnic uses of Sargassum oligocystum algae for healing of some diseases which have similar metabolic mechanism to the diabetes, its anti-diabetic effects in animal model was proposed.
The animals (rat) were divided into the normal control, diabetic control, positive control and, the test groups. The test groups were gavaged with oral doses of 150 and 300 mg/kg of algae hydroalcoholic extracts. After 30 days of intervention the serum glucose, cholesterol, triglyceride, HDLC, LDLC, insulin, insulin resistance, β-cells function and, the histopathology of pancreatic tissue were evaluated.
In animals that were fed with algae extracts a significant decrease in the fasting blood glucose, triglyceride and HOMA-IR and an increase in the HOMA-B with no significant impacts on the insulin, cholesterol and HDL were observed. Also, the histopathology evaluations in the groups which were treated with algae extract revealed the regeneration and reconstitution of damaged pancreatic β-cells.
The results give evidence that, the S. oligocystum algae extract has a healing effect on diabetes which can be considered as a new research prospect for the natural therapy of diabetes.

Some reports have shown neuroprotective effects of caffeine in several neurodegenerative disorders. However, its mechanism of action is not completely clear. Therefore, the aim of this study was to explore the interference of ryanodine, N-methyl-D-aspartate (NMDA) and adenosine modulators with the neuroprotective effects of caffeine against β-amyloid (Aβ) neurotoxicity in the SHSY5Y cells. The SHSY5Y cells were treated with Aβ23-35 (20µM) and/or caffeine (0.6 and 1mM), or both for 24 hours. Adenosine (20, 40, 60, 80, 100µM), NMDA (20, 50, 70, 90µM), dantrolene (2, 4, 6, 8, 10µM) were also added to the medium and incubated for 24 hours. The cell viability was measured via the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) method. The data were analyzed using one-way ANOVA followed by Bonferroni test. Caffeine at all the used concentrations (0.6, 0.8, 0.9, 1, and 3mM) significantly protected neuronal cells against Aβ neurotoxicity. Adenosine at the concentrations of 20, 40, 80 and 100μM diminished the neuroprotective effects of caffeine (0.6 and 1mM) against Aβ neurotoxicity. NMDA at the concentrations of 20, 50, 70 and 90μM blocked caffeine (0.6 and 1mM) neuroprotective effects. Dantrolene at the concentration of 2, 4, 6, 8 and 10μM diminished the neuroprotective effects of caffeine (0.6mM) and at the concentrations of 2 and 10μM impede caffeine (1mM) neuroprotection against Aβ neurotoxicity. Caffeine produced neuroprotective effect against Aβ neurotoxicity. Blockade of adenosine and NMDA receptors, as well as the activation of ryanodine receptors, may contribute to the neuroprotective effects of caffeine.

The present study aimed at comparing the prevalence of major psychiatric disorders including major depressive disorder, bipolar disorder, schizophrenia, and generalized anxiety disorder between performance-enhancing drug users and nonuser bodybuilders. Moreover, the prevalence of major psychiatric disorders in bodybuilders was also reported.
In this study, 453 athletes were recruited from Bushehr bodybuilding gyms from February to May 2015. A structured questionnaire was used to collect the participants’ information, including demographic characteristics, sports’ status and performance-enhancing drug use. According to the condition of performance-enhancing drug use, the participants were divided into current users, non-current users, and nonusers. The psychiatric status of the participants was evaluated using DSM-IV diagnostic criteria for major depressive disorder, bipolar disorder, generalized anxiety disorder, and schizophrenia. We also asked about the acute psychotic disturbances after using performance-enhancing drugs, alcohol use, and history of aggressive behavior in bodybuilders. Data were analyzed using one-way analysis of variance and chi-square tests.
Prevalence of major depressive disorder, bipolar disorder, schizophrenia, generalized anxiety disorder, and the overall prevalence of psychiatric disorders in the bodybuilders was 19.7%, 3.8%, 1.5%, 16.6%, and 26.7%, respectively. After using performance-enhancing drugs, 33% of the bodybuilders had experienced acute psychological disturbances. There were no significant differences between current, non-current, and nonuser bodybuilding athletes in the measured psychiatric disorders.
Prevalence of psychiatric disorders was not significantly different in performance-enhancing drug users and nonusers. Thus, it can be concluded that performance-enhancing drugs do not increase the risk of psychiatric disorders in bodybuilders.

The current study aimed at evaluating testis parameters and spermatogenesis changes in male rats administrated by different busulfan doses and time to construct a subfertile animal model by stereological methods. In the present study, 150 male Wistar rats randomly divided into 5 groups. All experimental groups were treated by different concentrations of busulfan (0.0, 2.5, 5, 10, and 15 mg/kg). Rats were sacrificed 1, 15, and 30 days after busulfan treatment. The tissue processing was done for stereological study and the results were analyzed by the one-way ANOVA followed by the Duncan test. The most stereological parameters such as testes weight and volume, tubules volume density, interstitial tissue (P<0.05), and germinal epithelium (P<0.01) were significantly reduced by busulfan treatment. Also, at different busulfan doses, the number of spermatogenic cells including spermatogonia (P<0.05), spermatocyte, round and elongated spermatid, and the Sertoli and Leydig cells (P<0.01) significantly decreased, compared with those of the control group. The decline was more obvious in higher busulfan doses and time (from the day 15 to 30) (P<0.05). Most of testicular stereological parameters reduced during 15 days onwards after busulfan treatment in a dose-dependent manner.

Several reports have implied progressive increase of performance-enhancing drug (PED) use among Iranian athletes. More importantly, most of the previous research in the Iranian population had mainly focused on the anabolic steroid abuse, and ignored other agents..
The aim of this study was to investigate the prevalence and characteristics of PED use among bodybuilding athletes in Bushehr, south of Iran..
Four hundred and fifty three male bodybuilding athletes were recruited from Bushehr gyms between February and May of 2015. Men were eligible to participate in the survey if they had regularly participated in the strength-training exercise (minimum of 1 year and 4 hour/week). Data were collected via a face-to-face interview. The survey consisted of three separate parts including demographic data, exercise pattern and PED use..
According to this study, 234 (51.7%) of bodybuilding athletes had used PEDs. The PED users reported an average of 3.80 ± 4.52 agents’ use in their programs and they had used PEDs for the average of 3.24 ± 3.99 years. The most prevalent agents which had been abused by the athletes were anabolic steroids (used by 185 athletes (79.4% of athletes). Furthermore, 110 (47%) of athletes reported stimulant agents’ use during their routines. The most prevalent motivation for using PEDs was increasing muscle mass that was reported by 164 (70.1%) of PED users. In addition, sexual and dermatologic effects were the most prevalent adverse effects reported by the PED user athletes (114 (49.4%) and 103 (44.2%), respectively)..
This study showed the high rate of PED use among recreational and professional Iranian bodybuilding athletes that can expose them to the serious side effects of these agents..

Ryanodine receptor abnormalities has implicated in the generation and maintenance of seizure. Dantrolene, a selective ryanodine receptor antagonist, may be a potential drug for the prevention of seizure. Therefore, we aimed to clarify the protective effects of dantrolene against pentylenetetrazole seizure in mice. Male albino mice were received an intra-peritoneal injection of pentylenetetrazole (80 mg/kg) in seven separate groups (n=8). We used dantrolene (10,20 and 40 mg/kg), caffeine (200 mg/kg), dantrolene (40 mg/kg) caffeine (200 mg/kg), diazepam (5 mg/kg as a positive control) and vehicle 30 minutes before the injection of pentylenetetrazole. Then, we registered the latency time of the first seizure, the severity of seizures and the incidence of seizure and death. Kruskal-Wallis test followed by Mann-Whitney and Fisher’s exact test were used to analyze the data. Dantrolene (10,20 and 40 mg/kg) significantly increased the latency time for the first seizure. Furthermore, dantrolene (20 and 40 mg/kg, but not 10 mg/kg) attenuated the severity of seizures in comparison to the vehicle group. Moreover, dantrolene only at the dose of 40 mg/kg prevented from tonic-clonic seizure and death in comparison to the vehicle group. In contrast, the addition of caffeine abolished the protective effects of dantrolene on the tonic-clonic seizure/death and inhibited the beneficial effects of dantrolene on the severity of pentylenetetrazol seizures. The acute dantrolene administration produced an anticonvulsant effect in the pentylenetetrazole-induced seizure. Moreover, caffeine prevented from dantrolene anticonvulsant effects. These results may imply about ryanodine receptors and intracellular calcium roles in the generation and control of pentylenetetrazole seizure.

The level of serum uric acid, as an important endogenous antioxidant, may be correlated to the different phases of mood disorders.
The aim of this study was to compare serum uric acid levels before and after treatment in patients with acute mania and depression.
Patients and We measured serum uric acid in 33 manic and 10 depressed hospitalized patients, both before and after treatment. Mood disorder was diagnosed according to the DSM-IV criteria. Manic or depressive scores were measured with the Young Mania Rating Scale or the Hamilton Depression Rating Scale, respectively. Uric acid levels were compared in the acute and remission phases of the mood disorder, and the relationship of uric acid levels with the onset of response was analyzed.
Serum uric acid levels were increased after bipolar disorder treatment. Serum uric acid levels were increased after bipolar disorder treatment. Moreover, depressed patients with lower uric acid levels had a faster onset of response. The uric acid levels in the acute mania patients were higher than in the acute depression patients.
The remission phase, in comparison to acute mania or depression, had higher levels of uric acid. Moreover, lower serum uric acid may correlate to a faster response in depressed patients. These results may support the roles of the purinergic system and of oxidative stress in the treatment of mood disorders.

Theneuroprotective effect of lithium has been attributed to its therapeutic action. However, the role of glial cells particularly astrocytes, and the possible interactions between neurons and astrocytes in neuroprotective effects of lithium have been disregarded. Thus, the aim of this study was to evaluate the direct effects of lithium on brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (GDNF) in rat primary neuronal, astrocytes, and mixed neuro-astroglial cultures to assess the possible effects of lithium on astrocytes and neuro-astroglia interactions. Rat primary astrocyte, neuronal and mixed neuro-astrocyte cultures were prepared from cortices of 18-day embryos. Cell cultures were exposed to lithium (1 mM) or vehicle for 1 day (acute) or 7 days (chronic). BDNF and GDNF mRNA and protein levels were determined by RT-PCR and ELISA, respectively. Chronic but not acute lithium treatment increased intracellular BDNF and GDNF protein levels in rat primary neuronal and astrocyte cultures, respectively (P<0.05). However, chronic lithium treatment had no significant effect on intracellular BDNF protein level in astrocyte and mixed neuron-astrocyte cultures or GDNF protein levels in mixed neuron-astrocyte culture. Furthermore, acute and chronic lithium treatment had no significant effect on mRNA and extracellular BDNF and GDNF protein levels in three studied cultures. Present study showed that chronic lithium treatment affected neurotrophins both in neurons and astrocytes in a cell-type specific manner with no effect on neuron-astrocyte interactions. The findings of this study also highlighted the importance of astrocytes as drug targets involved in the neuroprotective action of lithium.

Free radicals generated by ionizing radiation attack various cellular components such as lipids. The lung is a very radiosensitive organ and its damage is a doselimiting factor in radiotherapy treatments. Melatonin (MLT), the major product of the pineal gland acts as a radioprotective agent. This study aims to investigate the radioprotective effects of MLT on malondialdehyde (MDA) levels and histopathological changes in irradiated lungs. In this experimental study, a total of 62 rats were divided into five groups. Group 1 received no MLT and radiation (unT), group 2 received oral MLT (oM), group 3 received oral MLT and their thoracic areas were irradiated with 18 Gy (oMR), group 4 received MLT by intraperitoneal (i.p.) injection and their thoracic areas were irradiated with 18 Gy (ipM-R), group 5 received only 18 Gy radiation in the thoracic area (R). Following radiotherapy, half of the animals in each group were sacrificed at 48 hours for evaluation of lipid peroxidation and early phase lung injuries. Other animals were sacrificed in the eighth week of the experiment for evaluation of the presence of late phase radiation induced lung injuries. Pre-treatment of rats with either i.p injection (p<0.05) and oral administration of MLT (p<0.001) significantly reduced MDA levels in red blood cell (RBC) samples compared to the R group. Furthermore, i.p. injection of MLT decreased MDA levels in plasma and tissue (p<0.05). In the early phase of lung injury, both administration of MLT significantly increased lymphocyte (p<0.05) and macrophage frequency (p<0.001). MLT reduced the lung injury index in the lungs compared to the R group (p<0.05). The result of this study confirms the radioprotective effect of MLT on lipid peroxidation, and in both early and late phases of radiation induced lung injuries in an animal model.

S100ß a neurotrophic factor mainly released by astrocytes, has been implicated in the pathogenesis of bipolar disorder. Thus, lithium may exert its neuroprotective effects to some extent through S100ß. Furthermore, the possible effects of lithium on astrocytes as well as on interactions between neurons and astrocytes as a part of its mechanisms of actions are unknown. This study was undertaken to determine the effect of lithium on S100β in neurons, astrocytes and a mixture of neurons and astrocytes. Rat primary astrocyte, neuronal and mixed neuro-astroglia cultures were prepared from cortices of 18-day''s embryos. Cell cultures were exposed to lithium (1mM) or vehicle for 1day (acute) or 7 days (chronic). RT-PCR and ELISA determined S100β mRNA and intra- and extracellular protein levels. Chronic lithium treatment significantly increased intracellular S100β in neuronal and neuro-astroglia cultures in comparison to control cultures (P<0.05). Acute and chronic lithium treatments exerted no significant effects on intracellular S100β protein levels in astrocytes, and extracellular S100β protein levels in three studied cultures as compared to control cultures. Acute and chronic lithium treatments did not significantly alter S100β mRNA levels in three studied cultures, compared to control cultures. Chronic lithium treatment increased intracellular S100ß protein levels in a cell-type specific manner which may favor its neuroprotective action. The findings of this study suggest that lithium may exert its neuroprotective action, at least partly, by increasing neuronal S100ß level, with no effect on astrocytes or interaction between neurons and astrocytes.