Nitrate levels in vegetables from markets in Tehran, Iran.

This study is aimed at measuring nitrate levels in different vegetables from Tehran's markets that are consumed raw and fresh and to evaluate human health risk. Basil, parsley, radish leaves, cress, leek, radish, spring onion were randomly collected from local markets and the nitrate content was analysed by spectrophotometry. Average nitrate levels in the samples were 40.1, 45.2, 50.0, 51.8, 55.4, 90.2 and 110 mg kg-1 in parsley, leek, basil, radish leaves, cress, radish and spring onion, respectively. The average content in all samples was below Iranian standard limits. Tuber vegetables had significantly higher nitrate content than (green) leafy vegetables.

Bisphenol A in dairy products, amount, potential risks, and the various analytical methods, a systematic review.

This systematic study deals with the amount of bisphenol A (BPA) in milk and dairy products, its analytical methods, and risk assessment. Milk is one of the drinks that has a high consumption. Bisphenol A can be present both in raw milk and its amount undergoes changes during the pasteurization process. This review was conducted by searching for the keywords Bisphenol A, BPA milk, dairy product, cheese, cream, butter, yogurt, measurement, detection, and analysis in different databases. The search was done in three databases, Scopus, PubMed and Science Direct. The largest number of studies on the determination of bisphenol A belonged to Asian and European countries. The amount of bisphenol A in milks was observed in the range from ND to 640 ng/mL. Furthermore, the amount of BPA in the tested cheese samples was observed in the ND range up to 6.1 ng/g and in the yogurt samples in the ND range up to 4.4 ng/g. The most used analytical method was based on liquid chromatography. The most used solvent for extraction was methanol or acetonitrile. HQ (Hazard Quotient) was also calculated in some studies. There was no risk in terms of milk consumption due to BPA contamination in extracted data.

Protective Effects of Glatiramer Acetate Against Paclitaxel-Induced Peripheral Neuropathy in Rats: A Role for Inflammatory Cytokines and Oxidative Stress.

Chemotherapy-induced peripheral neuropathy (CIPN) is a major challenge for cancer patients who undergo chemotherapy with paclitaxel. Therefore, finding effective therapies for CIPN is crucial. Glatiramer acetate is used to treat multiple sclerosis that exerts neuroprotective properties in various studies. We hypothesized that glatiramer acetate could also improve the paclitaxel-induced peripheral neuropathy. We used a rat model of paclitaxel (2 mg/kg/every other day for 7 doses)-induced peripheral neuropathy. Rats were treated with either different doses of glatiramer acetate (1, 2, 4 mg/kg/day) or its vehicle for 14 days in separate groups. The mechanical and thermal sensitivity of the rats by using the Von Frey test and the Hot Plate test, respectively, were assessed during the study. The levels of oxidative stress (malondialdehyde and superoxide dismutase), inflammatory markers (TNF-α, IL-10, NF-kB), and nerve damage (H&E and S100B staining) in the sciatic nerves of the rats were also measured at the end of study. Glatiramer acetate (2 and 4 mg/kg) exerted beneficial effects on thermal and mechanical allodynia tests. It also modulated the inflammatory response by reducing TNF-α and NF-κB levels, enhancing IL-10 production, and improving the oxidative stress status by lowering malondialdehyde and increasing superoxide dismutase activity in the sciatic nerve of the rats. Furthermore, glatiramer acetate enhanced nerve conduction velocity in all treatment groups. Histological analysis revealed that glatiramer acetate (2 and 4 mg/kg) prevented paclitaxel-induced damage to the nerve structure. These results suggest that glatiramer acetate can alleviate the peripheral neuropathy induced by paclitaxel.

Evaluation of zinc oxide nanocomposite with Aloe vera gel for packaging of chicken fillet against Salmonella typhi and Salmonella para typhi A.

The growing demand for high food quality has been encouraging researchers in the food industry to apply biodegradable nanocomposites, which provide new opportunities and challenges for the advance of nanomaterials in the food industry. The objective of this study was to estimate the antibacterial activity and cytotoxicity effects of zinc oxide nanocomposite/zeolite (c/Zeo) with Aloe vera gel (AG) and its effect on the shelf life of chicken meat. The ZnONPs/Zeo was assessed using X-ray fluorescence (XRF) and field emission scanning electron microscopy (FE-SEM) analyses. The cytotoxicity effect of ZnONPs/Zeo was assessed by MTT assay. Then, the minimum inhibitory concentrations (MIC) and minimum bactericidal concentration (MBC) of ZnONPs/Zeo and ZnONPs/Zeo-AG against Salmonella typhi and Salmonella para typhi A were investigated. Also, the preservative effect of nanocomposites on chicken fillets was evaluated. The results showed that these nanocomposites have the least cytotoxicity effect, resulting in good biocompatibility with the host. The MIC and MBC values of ZnONPs/Zeo-AG were lower than the ZnONPs/Zeo against S. typhi and S. paratyphi A. Both ZnONPs/Zeo-AG and ZnONPs/Zeo caused a significant decrease in the bacterial count of the chicken fillets. So, by spraying on meat, the number of bacteria presented a sharper decline as compared with the control group, resulting in an approximately 3.3 and 3-log10 reduction over 48 h in the ZnONPs/Zeo-AG and ZnONPs/Zeo treatment samples, respectively. In conclusion, antimicrobial packaging with ZnONPs containing A. vera is a beneficial solution for preserving and improving the quality, safety, and shelf life of fresh meat products.

The aqueous extract of Artemisia Absinthium L. stimulates HO-1/MT-1/Cyp450 signaling pathway via oxidative stress regulation induced by aluminium oxide nanoparticles (α and γ) animal model.

BACKGROUND: This research aimed to evaluate the protective effects of Artemisia Absinthium L. (Abs) against liver damage induced by aluminium oxide nanoparticles (Al2O3 NPs) in rats, including both structural and functional changes associated with hepatotoxicity. METHODS: Thirty-six rats were randomly divided into six groups (n = 6). The first group received no treatment. The second group was orally administered Abs at a dose of 200 mg/kg/b.w. The third and fifth groups were injected intraperitoneally with γ-Al2O3 NPs and α-Al2O3 NPs, respectively, at a dose of 30 mg/kg/b.w. The fourth and sixth groups were pre-treated with oral Abs at a dose of 200 mg/kg/b.w. along with intraperitoneal injection of γ-Al2O3 NPs and α-Al2O3 NPs, respectively, at a dose of 30 mg/kg/b.w. RESULTS: Treatment with γ-Al2O3 NPs resulted in a significant decrease (P < 0.05) in total body weight gain, relative liver weight to body weight, and liver weight in rats. However, co-administration of γ-Al2O3 NPs with Abs significantly increased body weight gain (P < 0.05). Rats treated with Al2O3 NPs (γ and α) exhibited elevated levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), alanine transaminase (ALT), and aspartate aminotransferase (AST). Conversely, treatment significantly reduced glutathione peroxidase (GPx), catalase (CAT), total superoxide dismutase (T-SOD), and total antioxidant capacity (TAC) levels compared to the control group. Furthermore, the expression of heme oxygenase-1 (HO-1) and metallothionein-1 (MT-1) mRNAs, cytochrome P450 (CYP P450) protein, and histopathological changes were significantly up-regulated in rats injected with Al2O3 NPs. Pre-treatment with Abs significantly reduced MDA, AST, HO-1, and CYP P450 levels in the liver, while increasing GPx and T-SOD levels compared to rats treated with Al2O3 NPs. CONCLUSION: The results indicate that Abs has potential protective effects against oxidative stress, up-regulation of oxidative-related genes and proteins, and histopathological alterations induced by Al2O3 NPs. Notably, γ-Al2O3 NPs exhibited greater hepatotoxicity than α-Al2O3 NPs.

Association Between Non-alcoholic Fatty Liver Disease and Heavy Metal Exposure: a Systematic Review.

Non-alcoholic fatty liver disease (NAFLD) is a debilitating disease with adverse effects including cirrhosis and hepatocellular carcinoma. Heavy metals can cause severe dysfunction in different body organs including the liver. This review offers the study regarding the positive or negative association between heavy metals exposure and non-alcoholic fatty liver disease. The method used in this study is a systematic review based on searching in the PubMed, Scopus, and Science direct databases with the keywords of fatty liver, non-alcohol fatty liver, heavy metal, mercury, cadmium, arsenic, chromium, thallium, lead, iron, zinc, and nickel. There were 2200 articles searched in databases, and after assessment, 28 articles were selected. Positive association is established between arsenic, cadmium, iron, lead, mercury, and fatty liver disease. A negative relationship is found between zinc, copper, and progressive fatty liver disease. Furthermore, laboratory methods for NAFLD diagnosis were examined according to the obtained manuscripts. Among the different diagnostic methods, magnetic resonance imaging (MRI) is a sensitive method.

Evaluation of DNA methylation in BDNF, SLC6A4, NR3C1 and FKBP5 before and after treatment with selective serotonin-reuptake inhibitor in major depressive disorder.

Aim: To identify the DNA methylation status of related genes in major depressive disorder following selective serotonin-reuptake inhibitor treatment. Materials & methods: 45 patients with major depressive disorder and 45 healthy volunteers were considered experimental and control groups, respectively. High-resolution melting real-time PCR was implemented to evaluate DNA methylation. Results: After 100 days of selective serotonin-reuptake inhibitor treatment, methylation of promoter CpG sites of BDNF, NR3C1, FKBP5 and SLC6A4 was significantly reduced. Compared with before treatment, patients' Hamilton Depression Rating Scale scores were significantly reduced after selective serotonin-reuptake inhibitor treatment (p ≤ 0.0001). Conclusion: Based on the proven effect of antidepressants on DNA methylation and gene expression, these medications can improve the treatment process and reduce depression scores after treatment.

Effect of heat stress on DNA damage: a systematic literature review.

Thermal stress has a direct effect on various types of DNA damage, which depends on the stage of the cell cycle when the cell is exposed to different climate conditions. A literature review was conducted to systematically investigate and assess the overall effect of heat stress and DNA damage following heat exposure. In this study, electronic databases including PubMed, Scopus, and Web of Science were searched to find relevant literature on DNA damage in different ambient temperatures. Outcomes included (1) measurement of DNA damage in heat exposure, (2) three different quantification methods (comet assay, 8-hydroxy-2-deoxyguanosine (8-OHdG), and γ-H2AX), and (3) protocols used for moderate (31) and high temperatures (42). The evidence shows that long exposure and very high temperature can induce an increase in DNA damage through aggregate in natural proteins, ROS generation, cell death, and reproductive damage in hot-humid and hot-dry climate conditions. A substantial increase in DNA damage occurs following acute heat stress exposure, especially in tropical and subtropical climate conditions. The results of this systematic literature review showed a positive association between thermal stress exposure and inhibition of repair of DNA damage.

Evaluation of statins as a new therapy to alleviate chronotropic dysfunction in cirrhotic rats.

AIMS: Liver cirrhosis defines by regenerative nodules and fibrotic septa, causing a complication called cirrhotic cardiomyopathy (CCM) with chronotropic hypo-responsiveness. In addition to lowering cholesterol levels, statins yield antioxidant and anti-inflammatory effects. In liver diseases animal models, statins have been shown to decrease hepatic inflammation, fibrogenesis, and portal pressure (PP). Therefore, we evaluated the atorvastatin effect on the heart in cirrhotic rats. MATERIALS AND METHODS: Bile duct ligation (BDL) or sham operation performed on male Wistar rats and grouped as cirrhotic; BDL/Saline, BDL/Ator-7d(days) (Atorvastatin 15 mg/kg/day), and BDL/Ator-14d groups, or control; Sham/Saline, Sham/Ator-7d, and Sham/Ator-14d groups. Corrected QT interval (QTc interval), chronotropic responses, serum brain natriuretic peptides (BNP), heart tumor necrosis factor-α (TNF-α), nuclear factor erythroid 2-related factor 2 (Nrf2), and malondialdehyde (MDA) levels were studied along with atrial Ras homolog family member A (RhoA) and endothelial nitric oxide synthase (eNOS) gene expression. KEY FINDINGS: The chronotropic responses decreased in BDL/Saline and increased in BDL/Ator-7d group. The QTc interval, BNP, TNF-α, and MDA levels increased in BDL/Saline and decreased in BDL/Ator-14d group. The Nrf2 level did not change in BDL/Saline and increased in BDL/Ator-14d group. The liver inflammation and fibrosis increased in BDL/Saline and did not affect BDL/Ator-7d and BDL/Ator-14d groups. The RhoA expression was down-regulated in BDL/Saline, BDL/Ator-7d, and BDL/Ator-14d groups. The eNOS expression did not change in BDL/Saline and down-regulated in BDL/Ator-14d group. SIGNIFICANCE: Atorvastatin alleviates the chronotropic hypo-responsiveness and down-regulates the atrial RhoA and eNOS gene expression along with anti-inflammatory, antioxidant, and anti-stress effects in CCM.

Melatonin ameliorates disease severity in a mouse model of multiple sclerosis by modulating the kynurenine pathway.

Melatonin (MT), a neurohormone with immunomodulatory properties, is one of the metabolites produced in the brain from tryptophan (TRP) that has already strong links with the neuropathogenesis of Multiple sclerosis (MS). However, the exact molecular mechanisms behind that are not fully understood. There is some evidence showing that MS and MT are interconnected via different pathways: Relapses of MS has a direct correlation with a low level of MT secretion and a growing body of evidence suggest that MT be therapeutic in Experimental Autoimmune Encephalomyelitis (EAE, a recognise animal model of MS) severity. Previous studies have demonstrated that the kynurenine pathway (KP), the main pathway of TRP catabolism, plays a key role in the pathogenesis of MS in humans and in EAE. The present study aimed to investigate whether MT can improve clinical signs in the EAE model by modulating the KP. C57BL/6 mice were induced with EAE and received different doses of MT. Then the onset and severity of EAE clinical symptoms were recorded. Two biological factors, aryl hydrocarbon receptor (AhR) and NAD+ which closely interact in the KP were also assessed. The results indicated that MT treatment at all tested doses significantly decrease the EAE clinical scores and the number of demyelinating plaques. Furthermore, MT treatment reduced the mRNA expression of the KP regulatory enzyme indoleamine 2,3-dioxygenase 1(IDO-1) and other KP enzymes. We also found that MT treatment reduces the mRNA expression of the AhR and inhibits the enzyme Nicotinamide N-Methyltransferase (Nnmt) overexpression leading to an increase in NAD+ levels. Collectively, this study suggests that MT treatment may significantly attenuates the severity of EAE by altering the KP, AhR and NAD+ metabolism.

Deep eutectic solvent as the acceptor phase in three-phase hollow fiber liquid-phase microextraction for the determination of pyrethroid insecticides from environmental water samples prior to HPLC.

In this study, a deep eutectic solvent as the acceptor phase was applied in three-phase hollow fiber liquid-phase microextraction for the microextraction of two pyrethroids (permethrin as well as deltamethrin) from environmental water samples prior to HPLC-UV. A deep eutectic solvent was synthesized of tetrabutylammonium bromide-decanoic acid (in a ratio of 1:2) as an acceptor phase and 1-decanol was applied as a supported liquid membrane. Some main variables affecting the extraction recoveries, comprising the types/contents of extraction solvent and acceptor phase, stirring speed, sample phase pH and extraction time, were checked and optimized. Under optimal conditions, the detection limits and limits of quantitation determined were 0.09-0.12 and 0.29-0.39 µgl-1 for deltamethrin and permethrin, respectively. The enrichment factors were 627 and 613, while the relative standard deviations (n = 5) were 4.8 and 5.7%, for deltamethrin and permethrin, respectively. The created technique was assessed as satisfactory to ascertain the two pyrethroid poisons (permethrin and deltamethrin) in environmental water samples.

Thermal stress and TiO2 nanoparticle-induced oxidative DNA damage and apoptosis in mouse hippocampus.

Titanium dioxide (nano-TiO2) is used abundantly in various industrial products and novel medical therapies. In addition, the impact of climate change on the health and safety will undoubtedly increase in the future. However, the effects of exposure to these nanoparticles and heat stress on hippocampal DNA damage and apoptosis remain unclear. This study was conducted to evaluate the DNA damage and apoptosis in the hippocampal tissue and the physiological responses in mice induced by intraperitoneal (i.p.) administration of TiO2 nanoparticles (NPs) and heat stress for 14 consecutive days. The results showed that heat stress and TiO2-NPs were induced in the mouse hippocampus that led to hippocampal reactive oxygen species generation, oxidative damage of DNA, and apoptosis in a partly dose-dependent manner, especially at very hot temperature. High doses of nanosized TiO2 and severe heat stress significantly damaged the function of the hippocampus, as shown in the comet assay and apoptosis tests. The results of this study may provide data for appropriate measures to control and assess the risk of nano-TiO2 and thermal stress hazards to human health, especially workers. Safety guidelines and policies should be considered when handling nanomaterials in a hot environment.

Cardioprotective effects of sodium thiosulfate against doxorubicin-induced cardiotoxicity in male rats.

BACKGROUND: Doxorubicin (DOX) is an effective antitumor agent, but its clinical usage is limited due to adverse cardiotoxic effects. Several compounds have been studied to reduce DOX cardiotoxicity to improve its therapeutic index. This study was aimed to investigate the protective effects of sodium thiosulfate (STS) pre-treatment against DOX-induced cardiomyopathy in rats. METHODS: Male Wistar rats were randomized into 4 groups: control (saline), DOX (2.5 mg/kg, 3 times per week, intraperitoneal [i.p.]), STS (300 mg/kg, 3 times per week, i.p), and DOX + STS (30 min prior to DOX injection, 3 times per week, i.p.) over a period of 2 weeks. The body weight, electrocardiography, histopathology, papillary muscle contractility, and oxidative stress biomarkers in heart tissues were assessed. RESULTS: The results indicated that STS significantly improved the body weight (P < 0.01), decreased QRS complex and QT interval on ECG (P < 0.05 and P < 0.001, respectively), as well as declined the papillary muscle excitation, and increased its contraction (P < 0.01) compared to DOX-treated rats. STS strongly suppressed oxidative stress induced by DOX through the significant improvement of the cardiac tissue antioxidant capacity by increasing glutathione, superoxide dismutase (P < 0.001), and decreasing the level of lipid peroxidation (P < 0.01). CONCLUSION: Taken together, the results of this study demonstrated that STS showed potent cardioprotective effects against DOX-induced cardiotoxicity by suppressing oxidative stress.

Antibiotic treatment during pregnancy and lactation in dams exacerbates clinical symptoms and inflammatory responses in offspring with experimental autoimmune encephalomyelitis.

A growing body of evidence demonstrates that an imbalance in the intensive communication between gut microbiota and the host might be associated with immune-related disorders such as multiple sclerosis. This study set out to determine whether antibiotic treatment during pregnancy and lactation can affect the onset and severity of clinical symptoms and inflammatory responses in offspring with experimental autoimmune encephalomyelitis (EAE; a mouse model of multiples sclerosis). Female C57BL/6 mice received antibiotics or vehicles during pregnancy and lactation, then their offspring were induced with EAE in adulthood. We also measured interleukin (IL)-6, tumor necrosis factor (TNF)-α, interferon-gamma (IFN-γ), IL-17A, IL-10, and transforming growth factor (TGF)-ß in the serum of offspring. The findings indicate that antibiotic treatment in dams significantly exacerbated the severity of EAE clinical symptoms in both male and female offspring. However, antibiotic treatment only accelerated the onset of EAE disease in male but not female offspring. We did not find any significant changes in cytokines in non-EAE male and female offspring treated with antibiotics. Antibiotic treatment significantly enhanced levels of IL-6, TNF-α, IFN-γ, IL-17A, and TGF-ß in EAE-induced male offspring, and IFN-γ, IL-17A, and IL-10 levels in EAE-induced female offspring. There were also sex differences in the onset and severity of EAE disease, and inflammatory cytokines (IL-6, IFN-γ, and IL-17A) between EAE-induced male and female offspring treated with antibiotics. Taken together, this study suggests that antibiotic treatment during pregnancy and lactation in dams might affect the development of the immune system in male and female offspring in adulthood.

Montelukast suppresses the development of irritable bowel syndrome phenotype possibly through modulating NF-κB signaling in an experimental model.

Irritable bowel syndrome (IBS) is a functional gut disorder with multi-factorial pathophysiology that causes recurring pain or discomfort in the abdomen, as well as altered bowel habits. Montelukast, a well-known cysteinyl leukotriene receptor 1 (CysLT1R) antagonist, is widely used for the anti-inflammatory management of asthma. The present study aimed to evaluate the effects of pharmacological inhibition of CysLT1R on acetic acid-induced diarrhea-predominant IBS (D-IBS) in rats. Behavioral pain responses to noxious mechanical stimulation were decreased in the montelukast-treated rats as compared to the model animals following colorectal distension (CRD)-induced visceral hypersensitivity. Stool frequency decreased dose-dependently by montelukast in IBS rats exposed to restraint stress. A significantly shorter immobility time was also observed in IBS rats who received montelukast vs IBS group in the forced swimming test (depression-like behavior). Furthermore, there were significant decreases in the NF-κB protein expression, inflammatory cytokine (TNF-α, and IL-1ß) levels, and histopathological inflammatory injuries concomitant with increased anti-inflammatory cytokine, IL-10, in montelukast-treated rats compared with the IBS group. Cysteinyl leukotriene production and CysLT1R mRNA expression showed no remarkable differences among the experimental groups. The present results suggest the possible beneficial effects of montelukast in the management of D-IBS symptoms. The molecular mechanism underlying such effects, at least to some extent, might be through modulating CysLT1R-mediated NF-κB signaling. Yet, more studies are required to demonstrate the clinical potential of this drug for IBS therapy.

Sensing of oxidative stress biomarkers: The cardioprotective effect of taurine & grape seed extract against the poisoning induced by an agricultural pesticide aluminum phosphide.

Aluminum phosphide is a well-known hazardous agent used as an agricultural pesticide to protect stored grains from insect damage. However, accidental consumption of a trivial amount of it caused irreversible damage to the human body or even death in acute cases. The present study used taurine and grape seed extract as a natural cardioprotective medicine against aluminum phosphide poisoning by decreasing oxidative stress. The activity of oxidative stress biomarkers (Malondialdehyde, Catalase, Protein carbonyl, and Superoxide dismutase) were evaluated in the cell line model on Human Cardiac Myocyte cells. In the beginning, to clarify the pure impact of aluminum phosphide poison, taurine, and grape seed extract on the human heart cells, their effects on the biomarkers quantity in cell line were measured. Subsequently, the effect of taurine and grape seed extract with various concentrations as a treatment on the oxidative stress biomarkers of the poisoned heart cells were studied. Data analysis reveals that taurine and grape seed extract treatment can successfully diminish the poisoning effect by their antioxidant properties. The oxidative markers values of the poisoned cells were recovered by taurine and grape seed extracts treatment. Taurine (2 g/l) can recover Malondialdehyde, Catalase, Protein carbonyl, and Superoxide dismutase by 56%, 78%, 88%, 78%, when the recovering power of grape seed extract (100 g/l) for the aforementioned enzymes are 56%, 0.71%,74%, 51%, respectively. Therefore, it is clear that the performance of taurine in the recovery of the biomarkers' value is better than grape seed extract.

Neuroprotective effect of sumatriptan in pentylenetetrazole-induced seizure is mediated through N-methyl-D-aspartate/nitric oxide and cAMP response element-binding protein signaling pathway.

Seizure occurs as a result of uncontrolled electrical disturbances within the brain. Various biomolecules such as N-methyl-D-aspartate (NMDA), nitric oxide (NO), and cAMP response element-binding protein (CREB) have been implicated in the pathophysiology of seizure. Sumatriptan is a specific 5-Hydroxytryptamine 1B/1D receptor agonist and has neuroprotective effects in various neuropsychiatric disorders. In the current study, we tried to investigate the possible interaction of sumatriptan with NMDA/NO and CREB signaling pathway in PTZ induced seizure. For this purpose, various agonist and antagonist of NMDA such as MK-801 and Ketamine, NO precursor L-ARG, and NOS inhibitors L-NAME and 7-NI were co-administered with sumatriptan in PTZ induced seizure model. The level of nitrite in mice hippocampus was determined by Griess reaction. The gene expression of NR1, NR2A, NR2B, and CREB were quantified by quantitative real time-polymerase chain reaction (qRT-PCR). Furthermore, the involved neuronal nitric oxide synthase (nNOS) protein expression was examined via western blot analysis. Effective dose of sumatriptan (1.2 mg/kg) alone and subeffective dose of sumatriptan (0.3 mg/kg) in combination with NMDA and/or NO antagonist showed significant (P < 0.001) anticonvulsant activity in mice. Furthermore, sumatriptan significantly inhibited the PTZ-induced mRNA expression of NR2A (P < 0.0001), NR2B (P < 0.05), and CREB (P < 0.01). Also, the expression of nNOS protein in PTZ treated group was reversed by sumatriptan (P < 0.01). Hence, current findings suggest that the anticonvulsant effect of sumatriptan was due to down regulation of NMDA/NO and CREB signaling pathway.

Association of maternal lead exposure with the risk of preterm: a meta-analysis.

BACKGROUND: The relationship between maternal lead level and risk of preterm birth (PTB) remained controversial. Therefore, herein we performed this meta-analysis to investigate the association of maternal blood, urine and cord blood lead level with the risk of PTB using observational studies. METHODS: A systematic search was conducted in PubMed, EMBASE and Ovid Medline databases from inception to August 2019, and sixteen studies with 65600 participants investigating the association between maternal lead level and PTB were included in our meta-analysis. Odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated for the highest versus lowest lead level by random-effects model. RESULTS: Overall, the pooled OR of all included articles for the highest versus lowest PTB score was 1.29 (95% CI = 1.14-1.46; I2 = 80.4%, p < .001), and the results revealed a direct and significant relationship between second and third trimester blood lead level (BLL) and PTB (OR 2nd trimester= 1.61, 95% CI = 1.08-2.40, OR 3rd trimester= 1.57, 95% CI = 1.11-2.23). CONCLUSION: Results of this meta-analysis showed that maternal BLL is directly associated with the risk of PTB.

Glatiramer acetate attenuates depressive/anxiety-like behaviors and cognitive deficits induced by post-weaning social isolation in male mice.

RATIONALE: Major depressive disorder (MDD) is a debilitating disorder with adverse effects on mood, memory, and quality of life. OBJECTIVES: In this study, the antidepressant potential of glatiramer acetate (GA), a drug used in the management of multiple sclerosis, was investigated in acute and chronic models of depression in male mice. The acute antidepressant screening was performed with the forced swim (FST) and tail suspension (TST) tests. In the chronic phase, post-weaning social isolation (SI) was used to induce depressive-/anxiety-like behaviors. METHODS: Mice were reared in two different groups of social (SG) and isolated (IG) for 4 weeks. IG mice were treated with 0.5, 1.0, and 2.0 mg/kg of GA for the last 2 weeks of the SI period. Animals were assessed by the behavioral tests of depression, anxiety, learning, and memory, and hippocampal brain-derived neurotrophic factor (BDNF) level was measured. RESULTS: The acute tests confirmed the antidepressant potential of GA. In the chronic phase, GA could reduce immobility time in FST (P < 0.05), increase exploration activity in open field test (P < 0.05), increase open arms duration (P < 0.05) and entries in elevated plus maze (P<0.001), and improve memory and learning in passive avoidance test (P < 0.05). The BDNF level was increased in IG mice and decreased in IG mice treated with GA. CONCLUSIONS: Our results showed that GA improved depressive-/anxiety-like behaviors and cognitive dysfunction of SI reared mice without increasing the BDNF level which may be associated with other mechanisms of actions of GA.

Study of the cardioprotective effects of crocin on Human Cardiac Myocyte cells and reduction of oxidative stress produced by aluminum phosphide poisoning.

OBJECTIVES: The effects of Crocin as a cardioprotective material against Aluminum phosphide poisoning by reducing the oxidative stress is investigated. METHODS: The level of biomarkers of oxidative stress (Catalase, Superoxide dismutase, Malondialdehyde and Protein carbonyl) were measured in the cell culture model on Human Cardiac Myocyte cells to detect the protective effect of crocin. Initially, to define the pure impact of aluminum phosphide poison and crocin on the heart cells, their effects on the biomarkers quantity in cell line were measured, separately, using the standard related kits. Later the effect of crocin with different concentration as a treatment on the oxidative stress biomarkers of the poisoned heart cells were monitored. Note that in pre-treatment case, the crocin was initially added to the cells before poisoning them. Data were analyzed using the analysis of variance method. KEY FINDINGS: Results showed that crocin treatment reduced the aluminum phosphide (AlP) poisoning effect significantly. The treatment resulted in substantial deviation in the biomarkers of oxidative stress at the pre- and post-treatment phases for all groups. The oxidative markers values of the poisoned cells were recovered by crocin treatment. CONCLUSIONS: Crocin is proposed as a potentially powerful antioxidant to treat the cardiotoxicity caused by aluminum phosphide poisoning.