maliheh soodi

Echium amoenum Fisch. & C.A.Mey. has been used for the management of the common cold, inflammation, depression, anxiety, and fatigue. This study aimed to explore the anti-fatigue and antioxidant effects of aqueous extract of E. amoenum (AEEA) on a rat model of acute fatigue. After preparing for AEEA, 30 Wistar rats were divided into five groups of six animals. Group 1 received distilled water; Group 2 was treated with distilled water and underwent a forced swimming test (FST); Groups 3-5 rats were administered AEEA (250, 500, and 1000 mg/kg), and subsequently underwent FST. Then, the levels of some biochemical parameters and oxidative stress markers were measured in the serum and liver tissues of rats. AEEA treatment significantly augmented the swimming time of rats compared to the control group. AEEA-treated animals had increased serum glucose and decreased serum urea levels. AEEA diminished serum activities of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH). Treating the rats with AEEA activated superoxide dismutase (SOD) and catalase (CAT) and decreased total oxidant status (TOS) in serum. AEEA increased the levels of thiols and glutathione (GSH) as well as the activity of glutathione peroxidase (GPx) and CAT in the liver tissues. In the liver tissue, AEEA also induced the activity of SOD and reduced TOS. These results may suggest AEEA as a potential anti-fatigue natural product to ameliorate the adverse effects of acute fatigue on the body.

Paraoxonase 1 (PON1) is a high-density lipoprotein-associated enzyme with both aryl esterase and lactonase activity, and it possesses significant antioxidant and anti-inflammatory properties. PON1 hydrolyzes the active metabolites of several organophosphorus (OP) insecticides, including parathion, diazinon, and chlorpyrifos. This widely studied enzyme is recognized for its protective role against organophosphate poisoning and vascular diseases, as well as its potential as a biomarker for conditions related to oxidative stress, inflammation, and liver disease. However, limited knowledge exists regarding PON1 activity status following acute organophosphate intoxication. The aim of the present study was to investigate changes in serum PON1 activity after acute chlorpyrifos poisoning and its relationship with acetylcholinesterase (AChE) activity.

Rats were orally given a single dose of chlorpyrifos (160 mg/kg), and blood samples were collected before treatment, as well as at 6 and 96 hours post-treatment. We measured serum cholinesterase, paraoxonase, and arylesterase activity of PON1.

Signs of OP poisoning, including miosis, salivation, tremors, fasciculation, and paralysis, were observed following intoxication, accompanied by a significant inhibition of AChE activity. All symptoms resolved after 48 hours, and AChE activity returned to baseline levels at 96 hours. In contrast, paraoxonase and arylesterase activities progressively increased after 6h and 96h treatment respectively.

The results of our study indicated that serum cholinesterase activity and paraoxonase activity negatively associated in OP poisoning. Based on these findings, monitoring paraoxonase activity after OP intoxication may serve as a valuable biomarker for assessing intoxication.

Acetamiprid, a widely used neonicotinoid pesticide in agriculture, acts as a stimulant on nicotinic acetylcholine receptors, potentially causing neurotoxicity. Quercetin, a neuroprotective flavonoid found in fruits and vegetables, shows promise in mitigating neurological disorders. This study investigated quercetin's protective potential against acetamiprid-induced memory impairment. Male rats were divided into four groups: control, acetamiprid (40 mg/kg), quercetin (20 mg/kg), and a combination of acetamiprid and quercetin, administered orally for 28 days. Cognitive performance was assessed using the Morris water maze test; oxidative stress markers in the hippocampus were evaluated, along with histological analysis. Rats exposed to 40 mg/kg acetamiprid exhibited significant memory impairment. Notably, co-treatment with quercetin reversed this effect. Acetamiprid induced oxidative stress, as indicated by increased lipid peroxidation, reduced thiol content, and decreased catalase (CAT) enzyme activity. Simultaneous quercetin and acetamiprid administration effectively mitigated these oxidative stress markers. Histological analysis demonstrated quercetin's ability to prevent acetamiprid-induced hippocampal neuronal damage. Quercetin shows promise in ameliorating acetamiprid-induced memory deficits and neuronal damage, making it a potentially valuable nutraceutical, especially for individuals exposed to pesticides like agricultural workers.

The immune system is responsible for protecting the body against foreign and carcinogenic agents, and its weakness can lead to death. The genus Allium has been proposed as a suitable candidate for maintaining the homeostasis of the immune system, so in this study, we investigated the effects of hydroalcoholic extract of Allium jesdianum on various immune responses in mice.

In this experimental study, we investigated the effect of different doses (50, 100, and 200 mg/kg) of the hydroalcoholic extract of A. jesdianum on the immune system of 25 mice in four groups. Animal weight, spleen organ weight and their relative weight, blood lymphocytes, ability to produce antibodies by hemagglutination method, delayed hypersensitivity response, mitogenic power of lymphocytes using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) were investigated GraphPad Prism v9.5.0.730 x64 + v8.4.0.671 software was used for statistical calculations. Comparison between different groups was done using one-way ANOVA test and Tukey-Kramer posttest, and p > 0.05 was considered as a significant difference.

The results of this study show that A. jesdianum could not have an effect on the population of blood lymphocytes (p > 0.05) and general weight (p > 0.05), but the weight of the spleen (0.23 ± 0.22) and the relative weight of the spleen (0.96 ± 0.09) increased. Exposure to A. jesdianum caused a significant increase in the responses of the delayed hypersensitivity test after 24 hours (53.47 ± 8.27) and 48 hours (68.81 ± 11.34) compared to the control group. Also, A. jesdianum significantly increased the antibody titer compared to the control group (6.91 ± 0.17). In addition, A. jesdianum could increase the proliferation of spleen lymphocytes (7.71 ± 0.34). Also, at the doses of 100 mg/kg (1.49 ± 0.09) and 200 mg/kg (2.39 ± 0.12), it increased the proliferation response to LPS mitogen; while only at the dose of 200 mg/kg (2.46 ± 0.22) was able to increase the proliferative response to PHA mitogen.

It seems that A. jesdianum improves various factors of the immune system. Its effects include increasing the proliferation of spleen lymphocytes, delayed proliferative response, and antibody production. In general, A. jesdianum was able to strengthen various immune responses, including humoral immunity and cellular immunity.

Alzheimer’s disease (AD) is an age-dependent neurodegenerative disease. Beta-amyloid (Aβ)-induced neurotoxicity has a pivotal role in AD pathogenesis; therefore, the modulation of Aβ toxicity is the promising therapeutic approach to control the disease progression. Medicinal plants because of their multiple active ingredients are effective in complex diseases, such as AD. Therefore, several studies have studied medicinal plants to find an effective treatment for AD. Ferulago angulata is a medicinal plant with antioxidant and neuroprotective activity. The present study was done to assess the protective effect of the methanolic extract of Ferulago angulate on Aβ-induced toxicity and oxidative stress in PC12 cells.

The methanolic extract of aerial parts of the plant was prepared by the maceration method. PC12 cells were cultured according to a standard protocol. PC12 cells were incubated for 24 hours with Aβ alone, and Aβ in combination with various concentrations of the F. angulata extract. Cell viability was determined by the methyl thiazole tetrazolium (MTT) assay. Also, reactive oxygen species (ROS) production and the activity of acetylcholine esterase (AChE), glutathione peroxidase (GPx), and caspase-3 enzymes were measured. 

The extract dose-dependently protected PC12 cells against Aβ-induced cell death. Also, Aβ increased ROS production, AChE, and caspase-3 activity, and decreased the GPx activity, which all were ameliorated by F. angulata extract. 

F. angulata extract protects against Aβ-induced oxidative stress and apoptosis. These effects may be due to the antioxidant and anticholinesterase activity of the extract. It is recommended to assess F. angulata extract as an anti-AD agent.

  This study evaluated the acute and subacute toxicity of the Coriander Triphala tablet (CTT) in Wistar rats. 

The CTT was prepared according to the method described in our previous work. In the acute toxicity study, five female Wistar rats received 2000 mg/kg CTT and five female rats were administered distilled water as control. In the subacute test, sixty male and female rats were randomly divided into six groups. Three groups received 200, 500, and 1000 mg/kg of the tablet; the satellite group was treated with 1000 mg/kg of CTT, and controls received distilled water for 28 days. Body weights and food and water intake of rats were recorded. Toxicity signs were recorded and hematological, biochemical, and histopathological analyses were performed. 

 No remarkable toxic effect of the tablet was observed in the rats after receiving a single dose of 2000 mg/kg. This indicated that the median lethal dose (LD50) was more than 2000 mg/kg. In the subacute toxicity study, different doses of CTT didn’t change hematological parameters. However, the tablet increased the levels of cholesterol, creatinine, and aspartate aminotransferase (AST) in males and alanine aminotransferase (ALT) and AST in females at high doses. Histopathological evaluation of liver samples from both sexes showed congestion and hydropic degeneration of hepatocytes. Renal histopathology revealed varying degrees of tubular cell necrosis. 

 Our data indicated the toxic effects of CTT on the liver and kidney, suggesting the need for special precautions in administration of this medication to the patients.

Monoamine oxidase (MAO) enzymes abundantly found in the central nervous system (CNS) play an essential role in CNS disorders, so monoamine oxidase inhibitors (MAOIs) have been used for the treatment of neurological ailments such as depression, Parkinson’s, and Alzheimer’s disease. Therefore, finding the new selective MAOIs is still on the focus of researchers’ attention. This study aimed to evaluate MAO-A and MAO-B inhibitory effects of seven methanolic extracts of Iranian medicinal plants including Sanguisorba minor, Cerasus microcarpa, Ferulago angulata, Stachys pilifera, Amygdalus scoparia, Rosa canina, and Alhagi pseudalhagi.

The dried aerial parts of the plants were extracted with methanol by the maceration method. The inhibitory effects of extracts on MAO-A and MAO-B enzymes of rat brain mitochondria were measured by the fluorimetric method by using kynuramine as a substrate.

Among the extracts, S. minor (IC50 = 7.133 µg/mL) and C. microcarpa (IC50 = 49.53 µg/mL) were the most potent MAO-A and MAO-B inhibitors, respectively. A comparison of the IC50 value indicated that A. scoparia and S. pilifera had a higher affinity for MAO-A inhibition, whereas C. microcarpa and R. canina selectively inhibited the MAO-B enzyme. Moreover, F. angulata was recognized as a non-specific MAO inhibitor. The A. pseudalhagi and S. minor extracts did not show any MAO-B inhibitory effect.

Our study showed that studied extracts have different MAO-A and MAO-B inhibitory effects. Therefore, they can be used for the treatment of various CNS disorders; also, these extracts are an excellent source for finding new compounds with MAO-A or MAO-B inhibitory effects.

Neonicotinoids are a new type of insecticides that have been introduced to the poison market during the last three decades. Acetamiprid (ACT) is a neonicotinoid and widely used for controlling pests. It targets the liver as a toxic agent and damages hepatic tissues through oxidative stress mechanisms. Quercetin is a flavonoid with potent antioxidant and hepatoprotective activity and protects tissues from oxidative damages. Thus, this study is aimed to assess the protective effect of quercetin on acetamiprid-induced hepatotoxicity.

Thirty-six Wistar rats were classified into six groups including control, DMSO, ACT 20, ACT 40, quercetin, and ACT40+quercetin. All treatments were administered orally with gavage for 28 days. Alanine amino transferase (ALT), aspartate amino transferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzyme activity was measured in serum as biomarkers of hepatotoxicity. Lipid peroxidation, superoxide dismutase (SOD) enzyme activity and total thiol content were measured in hepatic tissues. Also, hepatic tissue sections were prepared and stained with hematoxylin and eosin and evaluated under optic microscope for any tissue injuries.

Findings showed that ACT, especially in high dose (40mg/kg), induced hepatic tissue destruction associated with increased hepatic enzyme activity, except ALP activity, in the serum. Besides, ACT increased the lipid peroxidation and decreased total thiol content and SOD activity, which indicates ACT-induced oxidative stress in hepatic tissues. Also, hepatic tissue injuries were observed in ACT-treated group. All these changes in liver were prevented by quercetin.

Because of strong antioxidant properties, quercetin can cope effectively with ACT-induced hepatotoxicity.

 Beta-amyloid peptide (Aβ) causes neural cell death and has a pivotal role in the progression of Alzheimer’s disease (AD). The prevention of Aβ-induced toxicity is a target for agents intend to treat Alzheimer’s disease. Our previous in vitro study indicated anti-cholinesterase and anti-oxidant activity of Amygdalus scoparia and Cerasus microcarpa methanolic extracts. In the present study, their neuroprotective effects against Aβ-induced toxicity are investigated.

 The methanolic extracts of the aerial parts of A. scoparia and C. microcarpa were prepared by the maceration method. In the culture, mature cerebellar granule neurons (CGNs) were exposed to Aβ alone or in combination with different concentrations of extracts and incubated for 24 hours, and cell viability was measured by the MTT assay. Oxidative stress markers and AChE activity were also measured. Then, the AChE activity of cultured neurons was measured after incubation with different concentrations of extracts. The LD50 values of extracts were estimated using the limit test.

 The co-incubation of C. microcarpa and A. scoparia extracts with Aβ protected CGNs against Aβ-induced cell death and ameliorated Aβ-induced oxidative stress. The AChE activity of cultured neurons was inhibited by both extracts in a dose-dependent manner. LD50 was estimated as being above 2000 mg/kg for both extracts.

 Both extracts attenuated Aβ-induced cell death by ameliorating oxidative stress. Also, the inhibitory effect of extracts on AChE activity might have been involved. Based on these results, these extracts may have therapeutic effects on Alzheimer’s disease.  However, further investigations are recommended.

Serum paraoxonase (PON1) is a potent antioxidant that is associated with the pathogenesis of several diseases. Also, it is reported that environmental factors can modulate the PON1 activity. In this study, the association between the Organophosphates (OP) exposure and plasma Paraoxonase/Arylesterase (PON1) activity and also OP-induced oxidative stress was investigated among pesticide manufacturing factory workers. In this cross-sectional study, Plasma cholinesterase (PChE) and RBC Acetylcholinesterase activity (AChE) were measured as a biomarker of OP exposure. Also, the amount of malondialdehyde (MDA) was evaluated as a biomarker for lipid peroxidation and oxidative stress. The PON1activity was measured by two distinct substrates, Paraoxson and Phenylacetate, to measure paraoxonase (PONase) and arylesterase (AREase) activities of PON1 enzyme respectively.  A significant decrease was observed inPChE and AChE activities in the blood sample of factory workers which confirmed OP exposure (p<0.001). Furthermore, the level of MDA increased that shown lipid peroxidation induced by OP (p<0.05). PONase and AREase activities decreased significantly in factory workers (p<0.05, p<0.001_). The reduction in AREase activity shown a correlation with the decrease in PChE and AChE activities (p<0.01), also a negative correlation was observed with AREase activity and lipid peroxidation (p<0.01). The Ponase activity only negatively correlated with lipid peroxidation (p<0.01). Our study indicates that occupational OP pesticide exposure in factory workers causes a decrease in serum PON1 activity which is associated with oxidative stress. Decreased PON1 activity is involved in the pathogenesis of several diseases such as cardiovascular disease then it is recommended that PON1 activity of OP-pesticide workers has been periodically monitored.

Alzheimer’s disease (AD) is an age-dependent neurodegenerative disorder and major cause of mortality in the elderly. AD has a complex pathophysiology and needs new multi-targeted compounds to halt the disease progression through several mechanisms. Medicinal plants contain various compounds with heterogeneous pharmacological effects, therefore are a good source. The aim of this study was to evaluate the protective effect of total extracts of Sanguisorba minor and Ferulago angulata on beta-amyloid (Aβ)-induced toxicity in primary neural cell culture. Cerebellar granule neurons (CGNs) were cultured according to standard protocols. The cultured neurons were incubated with Aβ alone or in combination with different concentrations of extracts for 24 hours. Cell viability was measured by methylthiazolyldiphenyl-tetrazolium (MTT) assay. In addition acetylcholinesterase (AChE) activity and oxidative stress markers were measured after incubation. Also, the effects of different concentrations of the extracts on AChE activity of the cultured neurons were investigated. For measuring the acute toxicity of the extract, LD50 was estimated by limit test. Both extracts could protect CGNs against Aβ-induced cell death. Aβ-induced oxidative stress and increase of AChE activity were ameliorated by both extracts. S. minor extract dose-dependently reduced AChE activity in cultured CGNs. LD50 of both extracts was estimated above 2000 mg/kg and considered as safe. Both studied extracts protected CGNs against Aβ-induced toxicity by ameliorating oxidative stress mechanism. According to these results, these extracts are recommended for further investigation in AD treatment.

Scopolamine, a muscarinic cholinergic receptor antagonist, is widely used to induce memory impairment in experimental animals. The present study aims to compare memory impairment and oxidative stress following single and repeated doses administration of scopolamine.
A group of rats received a single shot of scopolamine in different doses (0.5, 1, or 3 mg/kg, IP) 24 hours after the passive avoidance training. Then the memory retrieval test was performed 30 minutes and 7 days after the injection. In the other experiment, rats received similar doses of scopolamine for 7 consecutive days, 24 hours after the training session. Then the memory retrieval test was performed 30 minutes and 7 days after the last injection. Acetylcholinesterase (AChE) activity and lipid peroxidation were measured in their hippocampus tissue, too.
Scopolamine administered in repeated doses caused more impairment in memory function compared to single dose injection based on the evaluation 30 minutes after injection. Moreover, the memory impairment persisted for 7 days only in repeated doses treated groups. Increase in acetylcholinesterase activity and lipid peroxidation in both groups was observed 30 minutes after scopolamine administration. These abnormal increases persisted for 7 days only in repeated doses treated groups. Increased AChE activity and lipid peroxidation was well correlated with behavioral deficit. Also AChE activity was well associated with lipid peroxidation.
The results of present study showed that repeated administration of scopolamine induced results in memory impairment. This effect can be due to long-lasting oxidative stress which may damage the hippocampus tissue.

Alzheimer's disease (AD) is the most common form of dementia in the elderly. One of the major pathological hallmarks of AD is extracellular deposition of aggregated beta-amyloid (Aβ) peptide in the brain. Aβ causes neural cell death through several mechanisms. New treatments for AD focus on compounds that can modify disease progression and reduce symptoms through several mechanisms. Medicinal plants include several compounds with heterogeneous pharmacological effects that can be effective in the treatment of AD through different mechanisms. The aim of this study is to evaluate the protective effect of a methanolic extract of seven medicinal plants from Iran on Aβ induced toxicity in a cell culture model.
We cultured PC12 cells according to standard protocols. The cells were incubated with Aβ alone or with different concentrations of extracts for 24 hours. Cell viability was measured using the MTT assay.
Sanguisorba minor, Cerasus microcarpa, Ferulago angulate,andRosa caninasignificantly reduced Aβ-induced cell death in the PC12 cell culture. The observed protective effects of extracts were dose-dependent. We did not observe any protective effects with the Stachys pilifera,Amygdalus scoparia, and Alhagi pseudalhagi extracts.
Sanguisorba minor, Cerasus microcarpa,Ferulago angulate, andRosa canina extracts could be considered for treatment of AD.

Extracellular deposition of the beta-amyloid (Aβ) peptide, which is the main finding in the pathophysiology of Alzheimer’s disease (AD), leads to oxidative damage and apoptosis in neurons. Melissa officinalis (M. officinalis) is a medicinal plant from the Lamiaceae family that has neuroprotective activity. In the present study we have investigated the protective effect of the acidic fraction of M. officinalis on Aβ-induced oxidative stress and apoptosis in cultured cerebellar granule neurons (CGN). Additionally, we investigated a possible role of the nicotinic receptor.
This study was an in vitro experimental study performed on mice cultured CGNs. CGNs were pre-incubated with different concentrations of the acidic fraction of M. officinalis for 24 hours, followed by incubation with Aβ for an additional 48 hours. CGNs were also pre-incubated with the acidic fraction of M. officinalis and mecamylamin, followed by incubation with Aβ. We used the 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay to measure cell viability. Acetylcholinesterase (AChE) activity, reactive oxygen species (ROS) production, lipidperoxidation, and caspase- 3 activity were measured after incubation. Hochst/annexin V- fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining was performed to detect apoptotic cells.
The acidic fraction could protect CGNs from Aβ-induced cytotoxicity. Mecamylamine did not abolish the protective effect of the acidic fraction. AChE activity, ROS production, lipid peroxidation, and caspase-3 activity increased after Aβ incubation. Preincubation with the acidic fraction of M. officinalis ameliorated these factors and decreased the number of apoptotic cells.
Our results indicated that the protective effect of the acidic fraction of M. officinalis was not mediated through nicotinic receptors. This fraction could protect CGNs through antioxidant and anti-apoptotic activities.

Chlorpyrifos (CPF) is a neurotoxic organophosphorus (OP) insecticide. Its mechanism of action includes oxidative stress, excitotoxicity, and inhibition of the acetylcholinesterase enzyme (AChE). The aim of the present study is to investigate CPF toxicity in mature and immature cerebellar granule neurons (CGNs), as well as its effect on glutamate induced excitotoxicity.
This study was an in vitro experimental study performed on mice cultured CGNs. Immature and mature neurons were exposed to different concentrationsof CPF (1-1000 μM) and glutamate (10-600 μM) for 48 hours after which we used the MTT assay to measure cytotoxicity. Immature neurons had exposure to CPF for 5 days in order to evaluate the cytotoxic effect on developing neurons. Mature neurons received sub-lethal concentrations of CPF (10, 100 μM) combined with different concentrations of glutamate. AChE activity and reactive oxygen species (ROS) generation were assessed after treatments.
Immature CGNs had increased sensitivity to CPF toxicity compared to mature neurons. We observed significantly greater ROS production in immature compared to mature neurons, however AChE activity was more inhibited in mature neurons. Although CPF toxicity was not well correlated with AChE inhibition, it correlated well with ROS production. Glutamate toxicity was potentiated by sub-lethal concentration of CPF, however glutamate induced ROS production was not affected. The results suggested that CPF potentiated glutamate toxicity by mechanisms other than oxidative stress.
CPF toxicity differed in mature and immature neurons. Potentiated glutamate toxicity by CPF implied that CPF exposure might be a risk factor for neurodegenerative disease.

Hydroxymethylfurfural (HMF) is a common Maillard reaction product directly formed from dehydration of sugars under acidic conditions during heating and storage in carbohydrate rich foods. The aim of the present study was to detect and quantify the amount of HMF in date syrup by HPLC method. In addition, the amount of HMF in date syrup produced by traditional and industrial methods were compared.
A HPLC method for determination of HMF in date syrup was developed and validated. The amount of HMF in date syrup products produced by the traditional and industrial methods was compared. In addition, to determine whether HMF was produced during storage in date syrup, its amount was measured in fresh and old samples.
The HMF content of fresh traditional products varied between 1000 to 2675 mg⁄kg and in the old products varied between 2580 to 6450 mg⁄kg. The HMF concentration of the fresh industrial products varied between 12 to 456 mg⁄kg and 611 to 943 mg⁄kg in the old ones. The HMF concentration of the traditionally produced products was significantly higher than industrial products (P HMF was produced in date syrup during preparation and storage. Because HMF is recognized as an indicator of quality deterioration in a wide range of foods and is still under investigation for possible toxic effects, it is recommended that the amount of HMF is measured in date syrup and considered as an indicator of the quality control of this product.

Hexavalent chromium [Cr (VI)] compounds are well-known environmental contaminants generated from industrial processes. Several studies have reported the harmful effects of Cr (VI) on different organs, however, little is known about neurotoxic effects of Cr (VI). The aim of this study is to investigate the toxic effects of Cr (VI) on PC12 cells. PC12 cells were cultured following standard protocol and exposed to various concentrations (1-100 μM) of potassium dichromate (K2Cr2O7) for 24, 48 and 72 h. After exposure, cell viability was measured by the MTT assy. After exposure, production of reactive oxygen species (ROS) and lipid peroxidation were measured. Potassium dichromate induced significant cell death in PC12 cells. The IC50 values for cytotoxicity were 22.02 for 24 h, 1.88 for 48 h, and 1.85 for 72 h of exposure. Significant differences between IC50 for 24 h of exposure compared to 8 and 72 h of exposure were observed (p<0.05). ROS production and lipid peroxidation significantly increased in the Cr (VI) treated groups compared to the control group (p<0.05). The results indicated that Cr (VI) induced dose and time dependent cytotoxicity in PC12 cells which indicated neurotoxic effects of Cr (VI). Mechanisms of Cr (VI) induced toxicity have not been fully determined, however increased production of ROS and lipid peroxidation in Cr (VI) treated groups demonstrated that oxidative stress might be involved in neurotoxicity of Cr (VI).

Alzheimer’s disease (AD) is a neurodegenerative disease that was characterized with deposit of beta amyloid (Aβ) aggregate in senile plaque. Oxidative damage to neurons and loss of cholinergic neurons in forebrain region are observed in this disease. Melissa officinalis is a medicinal plant from Lamiaceae family, used traditionally in the treatment of cognitive disorders. It has cholinomimetic and potent antioxidant activity. In the present study, we investigated the possible neuroprotective effects of total ethanolic extract, acidic and non-acidic fraction of Melissa officinalis on Aβ-induced cytotoxicity and oxidative stress in PC12 cells and also measured their in-vitro anticholinesterase activity. PC12 cells were incubated with the extract and fractions prior to the incubation with Aβ and cell toxicity was assessed by MTT assay. In addition, productions of reactive oxygen species (ROS), Malondialdehyde (MDA) as a biomarker of lipid peroxidation and glutathione peroxidase activity were measured. Pretreatment of cells with total extract and acidic fraction (not non-acidic fraction) had protective effect against Aβ-induced oxidative changes and cell death. In concentrations in which both total extracts of an acidic fraction showed neuroprotective effects, inhibition of cholinesterase activity was not significant. Then, the protective effects of Melissa officinalis total extract and acidic fraction were not attributed to their anticholinesterase activity. Acidic fraction showed more potent protective effect compared to the total extract, leading to the fact that polyphenolic compounds and terpenoic acids are the most effective components in the total extract concentrated in this fraction.

A high-performance liquid chromatography with ultraviolet detection (HPLC/UV) method which was used solid-phase extraction for cleanup, was developed for the determination of Azinphos methyl, Phosalone, Diazinon and Chlorpyrifos residues in fruits. A full factorial experimental design was used for development of HPLC condition and evaluation of effect of three factors (pH of mobile phase, percent of acetonitril in mobile phase and flow rate) on the retention time and resolution of peaks. The samples were extracted with Hexan/Aceton(50/50)and then is loaded onto a C18 end-caped SPE cartridge for further clean up. For SPE condition optimization, several solvents (acetonitril, dichloromethane, ethyl acetate and hexane) were tested as eluent and the best recovery was found with hexane. The optimum HPLC condition was achieved with acetonitril: water (60:40) as mobile phase, flow rate 1 ml/min, on C8 column. The standard calibration curves were linear between 0.05-1μg/ml for Azinphos methyl and 0.1-2 μg/ml for others. The hexan:acetone extraction followed by the C18 end-cap SPE cleanup provided recoveries of >70% for all of pesticides and removing the greatest number of sample matrix interferences.

Nitric oxide (NO) is thought to be involved in spatial learning and memory in several brain areas such as hippocampus. This study examined the effects of post-training intrahippocampal microinjections of 1400W as a selective iNOS inhibitor on spatial memory, in anesthetized and non-anesthetized situations in rats. In the present work, 4-day training trials of animals were conducted. Spatial memory was tested 48 hours after the drug infusions. For microinjection of 1400W into CA1 region of the hippocampus in conscious animals, guide cannula was implanted into the CA1 area and 1400W was infused after recovery from surgical anesthesia. In anesthetized animals, 1400W was microinjected directly into CA1 region by Hamilton syringe during anesthesia. After completion of training, 1400W (10, 50 and 100 µM/side) were microinjected bilaterally (1 µL/side) and testing trials were performed 48 h after drug infusions in both groups of cannulated and non-cannulated rats. Significant reduction was observed in escape latency and traveled distance in animals that received 1400W (100 µM/side, *p < 0.05) via cannula after recovery in comparison with control group. Also, microinjection of 1400W (100 µM/side) in post recovery phase caused a significant (***p < 0.001) reduction in time and distance of finding the hidden platform in comparison with anesthetized situation. These findings suggest that 1400W has a significant improvement on spatial memory and memory enhancement induced by iNOS inhibitor can be affected by anesthesia in a period of time.