Traditional medicinal plants are valuable sources of bioactive compounds, many acting synergistically and their therapeutic uses are increasingly recognized. In this study, we examined the antimicrobial activity, antioxidant potential, and phytochemical constituents of four traditional medicinal plants (Verbascum sinuatum, Amaranthus spinosus, Carduus getulus, and Heterotheca subaxillaris) from the Gaza Strip in Palestine. Hexane extracts of each species were used for phytochemical characterization using Gas Chromatography - Mass Spectrometry (GC-MS). The total phenolic and flavonoid contents (TPC and TFC) were measured, followed by the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay to examine the antioxidant activity. The antibacterial activity was assessed using the disc diffusion method. GC-MS analysis revealed that each species contained distinct lipophilic compounds. The major classes of components identified in V. sinuatum included saturated fatty acid esters, phenolic antioxidants, and a putative alkaloid. A. spinosus contained oxygenated monoterpenes, fatty acid derivatives, and aromatic compounds. C. getulus was characterized by monoterpenes, diterpenes, fatty acid derivatives, and phenolic antioxidants. H. subaxillaris primarily yielded terpenoids, fatty acid esters, and phenolic compounds. Quantitative phytochemical profiling revealed that H. subaxillaris exhibited the highest TPC and TFC among the four species. Hexane extracts of H. subaxillaris, A. spinosus, V. sinuatum, and C. getulus demonstrated measurable antioxidant activity and inhibitory effect against Staphylococcus aureus, Bacillus cereus, Escherichia coli, and Pseudomonas aeruginosa. Among the extracts, H. subaxillaris exhibited the strongest antioxidant and antibacterial activities followed, by V. sinuatum, C. getulus, and A. spinosus. These findings highlight the importance of phytochemical profiling in the discovery of new potential bioactive compounds and support future endeavors to isolate valuable metabolites, investigate their biosynthetic processes, and any structure-activity relationships.

BackgroundThe need to develop agricultural practices has intensified the search for natural alternatives to synthetic agrochemicals, with the aim of reducing the risks of these synthetic chemical compounds.AimThis study compared the allelopathic and phytotoxic effects of Sinapis arvensis hexanic extract of leaves and flowers on the germination and early growth of Triticum aestivum. These biological activities were evaluated in relation to the chemical profiles, α-amylase inhibitory activities, as well as the antioxidant and antimicrobial properties of the extracts.Materials and methodsThe phytochemical profiles of the two extracts were established by gas chromatography–mass spectrometry (GC–MS) and tested for antioxidant, antimicrobial, and enzymatic inhibitory properties. The experiment followed a completely randomized design with three independent replicates per treatment. For each extract type (leaf or flower) and concentration (0, 0.625, 1.25, 2.5, and 5 mg/mL), three replicate Petri dishes containing 100 seeds each were used for every treatment combination. Control seeds received distilled water with 5% Tween-20 as a vehicle control.Resultsleaf hexane extract was composed mainly of trans-geranylgeraniol, isocitronellol, and fatty acid methyl esters, while flower hexane extract contained abundant sesquiterpenes such as cubenol, cedrol, and caryophyllene. Both hexanic extract of leaves and flowers exerted concentration-dependent inhibitory effects on seed germination, radicle and hypocotyl elongation, and seedling biomass, with the leaf hexane extract being remarkably more potent. The highest concentration (5 mg/ml) of leaf and flower extracts significantly reduced seed germination as well as radicle and hypocotyl growth (length and weight) compared to the control group. Notably, the extracts significantly decreased α-amylase activity in a dose-dependent manner. Moreover, both extracts showed moderate antioxidant activity with the flowers being more effective in radicals’ scavenging and exhibited antimicrobial effects mainly against Gram-positive bacteria.Summary and conclusionOverall, these findings demonstrate that S. arvensis is a rich source of bioactive secondary metabolites with potent allelopathic potential. The observed phytotoxic, antioxidant, and antimicrobial effects provide a mechanistic basis for understanding this allelopathic activity and its potential role in plant–plant interference.

Abamectin (ABM) is a macrocyclic lactone insecticide that induces oxidative stress and testicular toxicity, but its specific effects on male reproductive function remain unclear. Here, we tested whether an aqueous extract of Salvia officinalis (S. officinalis) could mitigate ABM-induced testicular injury in adult male rats, focusing on mitochondrial fusion and apoptosis. Thirty-six rats were divided into six groups: control, S. officinalis extract (100 mg/kg), low-dose ABM (0.5 mg/kg), high-dose ABM (1 mg/kg), S. officinalis + low-dose ABM, and S. officinalis + high-dose ABM, for 70 days. Our results showed that the extract was rich in total phenolics and flavonoids. The main phenolic compounds were ferulic acid, syringic acid, caffeic acid, p-coumaric acid, and α-tocopherol, while the main flavonoids were luteolin, 2'-hydroxyflavone, apigenin, and quercetin. Rats exposed to ABM had lower sperm concentration and motility, more abnormal sperm, and markedly lower serum levels of testosterone, luteinizing hormone, and follicle-stimulating hormone in a dose-dependent manner. Furthermore, testicular malondialdehyde and nitric oxide levels increased, whereas catalase activity, glutathione levels, and the activities of superoxide dismutase and glutathione S-transferase decreased. Gene expression analysis showed reduced mitofusin-1 and mitofusin-2 and increased p53 and caspase-9 expression. Notably, co-administration of S. officinalis with ABM improved sperm quality, hormone levels, antioxidant status, gene expression, and testicular tissue structure. Our findings highlight the protective mechanisms of S. officinalis, including enhancing antioxidant defenses, promoting mitochondrial fusion, and inhibiting the intrinsic apoptotic pathway. These results suggest that the S. officinalis extract could have therapeutic potential for ABM-induced male reproductive toxicity.

Lambda-cyhalothrin (LCT), a type II pyrethroid, is known to cause several side effects, including hepatorenal toxicity, despite its widespread use. This study investigates the protective effect of carvacrol (CVR) against LCT-induced oxidative stress, inflammation, and apoptotic pathway in the liver and kidney. Forty-eight male Sprague-Dawley rats were randomly assigned to eight groups; the first two groups served as controls (negative and CVR). The third, fourth, and fifth groups received LCT at doses of 2, 4, and 8 mg/kg/day via gavage. The sixth, seventh, and eighth groups received a dose of CVR (50 mg/kg/day) during LCT exposure for 90 days. Co-treatment with CVR reduced the elevated levels of hepatic biomarkers (alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and γ-glutamyl transferase (GGT)), kidney markers (urea and creatinine), and various histopathological changes caused by LCT exposure. Additionally, CVR mitigated LCT-induced oxidative stress by lowering malondialdehyde (MDA) levels, increasing cellular antioxidant (glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR)), and upregulating the transcription of the Trx1 and Prx1 genes. Moreover, CVR decreased the pro-inflammatory cytokine (tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6)) levels, along with the activation of apoptotic markers (p53, Bax, and caspase-3), and lowered Bcl2 levels. Furthermore, the in silico study confirmed that LCT interacts directly with the active cysteine residues of Trx1, Prx1, and Bcl2 proteins at high binding energies. In conclusion, sub-chronic exposure to LCT can induce hepatorenal apoptosis by inhibiting the Trx1/Prx1/Bcl2 pathway, an effect that is reversed by CVR's antioxidant properties.

Bisphenol A (BPA), a common endocrine-disrupting chemical, can cause oxidative damage, apoptosis, and necroptosis in various organs. However, the underlying mechanisms for BPA-induced neurotoxicity were not properly reported. Here, we have evaluated the possible ameliorative roles of astaxanthin (ASX) against BPA-induced brain apoptosis/necroptosis in male rats. Forty male rats were equally grouped (30 days) into control, ASX (75 mg/kg), BPA (50 mg/kg), and BPA/ASX (50 mg/kg/BAP+75 mg/kg/ASX). The present findings demonstrated that ASX could mitigate the diminished acetylcholinesterase (AchE) activity and the increased dopamine, serotonin, and norepinephrine levels, besides anxiety behaviors that resulted from BPA intoxication. Furthermore, ASX significantly reduced BPA-induced brain oxidative injury by mitigating malondialdehyde (MDA), glutathione (GSH), glutathione transferase (GST), superoxide dismutase (SOD), and catalase (CAT) levels. Moreover, ASX could alleviate the histopathological changes promoted by BPA and repair the transcript levels of p53, BcL2, caspase9, FADD, RIPK1/3, MLKL along with Bax, and caspase3 immunoreactivity. In conclusion, ASX reserved brain injury-induced apoptosis, and necroptosis following exposure to BPA through p53/Bcl2/Bax/caspase9/capasase3 and RIPK1/FADD/RIPK3/MLKL pathways.

Abstract Background The humanized monoclonal antibody galcanezumab is an anti-calcitonin-gene-related-peptide (CGRP) and frequently used for migraine prevention. However, the literature revealed limited data with conflicting results. This study aims to assess the safety and efficacy of galcanezumab in treating patients with episodic or chronic migraine. Methods We searched for randomized controlled trials till September 2022 from six databases (Cochrane library, Embase, PubMed, Web of Science, Scopus, and Clinicaltrials.gov registry). Our primary outcomes were the change in the number of monthly migraine headache days (MHDs) and adverse events. We extracted the data and analyzed it by RevMan (5.4) software. Results Eight studies with 4964 patients were included. Galcanezumab (≥ 120 mg) significantly reduced the MHDs for six months in migraine patients compared to placebo. The monthly risk ratio (RR) ranged from − 2.33 to − 1.62 for episodic migraine and − 2.86 to − 2.44 for chronic migraine. The response rate of ≥ 50%, ≥ 75% and 100% were higher with galcanezumab groups. The rate ranged from 1.72 to 4.19 for episodic migraine and 1.84 to 2.47 for chronic migraine. It is generally safe except for injection site safety outcomes (erythema, reaction, pruritis, and swelling), the results were significantly higher with galcanezumab groups. It appears dose independent except for injection site reaction, which showed higher with galcanezumab 120 mg only. Furthermore, any adverse events, serious adverse events (SAE) and that led to discontinuation were higher with galcanezumab 240 mg. Conclusion Galcanezumab is effective in patients with episodic or chronic migraine after one to six months use. It reduced MHDs and had an effective response rate. Moreover, it is generally safe except for injection site adverse events, and SAE, especially with galcanezumab 240mg.

Magnetite nanoparticles have attracted the attention of researchers for biomedical uses, but their impacts on the reproductive system did not report. Here, we have studied the possible attenuation efficiency of quercetin against magnetite nanoparticles-induced apoptosis in ovarian. Forty female rats were divided equally into control, quercetin (100 mg/kg), magnetite nanoparticles (50 mg/kg), and magnetite nanoparticles+quercetin, where all rats received their doses for four weeks. Compared with the control, magnetite nanoparticles significantly reduced the serum hormonal levels (follicle-stimulating hormone, luteinizing hormone, estrogen, and progesterone) along with glutathione and superoxide dismutase in ovarian tissues. Moreover, magnetite nanoparticles markedly increased the ovarian malondialdehyde, and apoptotic gene expressions (Bax and caspase-3), and induced many histopathological changes. Significantly, co-treatment with quercetin markedly alleviated the hormonal profile, antioxidant disturbance, and ovarian apoptotic pathway of magnetite nanoparticles. Furthermore, our docking study revealed that quercetin could act as a caspase-3 inhibitor and allosteric agonist to follicle-stimulating hormone (Met520 and Val53), luteinizing hormone (Met517, Ala589, Ser604, and Lys595), estrogen (Met421, Phe425, and Ala350), and progesterone (Met759 and Met909) receptors. Those records reveal that the antioxidants and antiapoptotic characteristics are acceptable pointers for female infertility defenders of quercetin, especially during nanoparticle exposure.

Maternal exposure to zearalenone (ZEA), a mycotoxin, can impact fetal liver development. This study investigated the protective effects of carvacrol (CRV) against ZEA-induced fetal liver damage. Thirty-two pregnant rats were allocated to four groups (eight rats/group); control, CRV (75 mg/kg), ZEA (5 mg/kg), and co-treated group (ZEA + CRV). The animals were given their doses during the gestation period. Maternal exposure to ZEA revealed a significant increase in the malondialdehyde (MDA) level in the fetal liver. In contrast, glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities, besides glutathione (GSH) levels, were decreased in ZEA-intoxicated rats. Additionally, ZEA increased the expression of pro-apoptotic genes (P53, Bax, and caspase-9), elevated the immunoreactivity of caspase-3, decreased anti-apoptotic Bcl-2, and induced severe fatty degeneration, congestion, and necrosis in the fetal liver. The comet assays revealed significant DNA damage, as evidenced by reduced head DNA content and increased tail DNA content and tail moment in the ZEA-exposed rats. Surprisingly, co-treatment with CRV significantly mitigated fetal hepatic lipid peroxidation, antioxidant disturbance, apoptosis, and DNA damage after maternal exposure to ZEA. These findings highlight the potential of CRV as a promising approach to mitigate ZEA-associated developmental hepatotoxicity.

Objective: In this systematic review and meta-analysis, we aimed to assess the efficacy and safety of galcanezumab doses in chronic and episodic migraines. Background: Migraine is a severe kind of headache and is represented by 14% of the population and up to 18% of women. Galcanezumab is a humanized monoclonal antibody that binds to calcitonin gene-related peptides and is used to prevent migraines. Design/Methods: In September 2022, we conducted a comprehensive search in five databases, including EMBASE, PubMed, Cochrane Library, Web of Science, and SCOPUS. We appraised each study using the Cochrane risk of bias tool. Our primary outcome was the change in the monthly migraine headache days (MMDs). Data were extracted and analyzed using RevMan version 5.4. Results: We included eight randomized controlled trials with 3651 migraine patients. In episodic migraine, galcanezumab (120–150 and 240–300mg) showed a significant reduction in MMDs compared to placebo after six months. Also, in chronic migraine, galcanezumab (120mg) reduced MMDs compared to placebo after three months. The analysis was conducted according to each month's records, and the mean difference change ranged from −1.62 to −2.86 (P-value < 0.001). All doses showed a significantly higher rate in ≥50%, ≥75%, and 100% response rates. Regarding safety outcomes, galcanezumab was associated with injection site-related complications such as pruritis, reaction, swelling, or erythema. In contrast, the two groups showed no difference regarding any adverse or serious adverse events, upper respiratory tract infection, oropharyngeal pain, injection site pain, back pain, sinusitis, and diarrhea. Conclusions: Subcutaneous galcanezumab reduced MMDs and increased response rates in chronic and episodic migraine patients. It is generally safe except for injection-related complications. Disclosure: Mohamed Sayed Zaazouee has nothing to disclose. Mr. Elsnhory has nothing to disclose. Ms. Ebrahim has nothing to disclose. Dr. Alaraj has nothing to disclose. Dr. Saad has nothing to disclose. Dr. Zaki has nothing to disclose. Mr. Ali has nothing to disclose. Dr. Fahmy Fawy has nothing to disclose. Dr. Ahmed has nothing to disclose. Dr. Elshennawy has nothing to disclose. Dr. Eleyan has nothing to disclose. Dr. Alahmad has nothing to disclose. Dr. Abo Hamra has nothing to disclose. Dr. AbuEl-Enien has nothing to disclose. Dr. Elromely has nothing to disclose. Dr. Elshanbary has nothing to disclose.

Background: Dupilumab is a human monoclonal antibody directed against the alpha subunit of the interleukin-4 receptor and inhibits the signaling of IL-4 and IL-13. It is approved for treating asthma and other type-2 inflammatory diseases. There is a conflict in the literature regarding the safety and efficacy of dupilumab. Thus, we aimed to assess the safety and efficacy of dupilumab in patients with moderate to severe asthma. Methods: Six databases (PubMed, Embase, Scopus, Web of Science, Cochrane library, and clinicaltrials.gov registry) were searched until January 2022. We included randomized controlled trials that compared dupilumab with the placebo in moderate to severe asthma patients. We extracted the data at 12 and 24 weeks and analyzed them using review manager 5.4. Findings: Thirteen trials were included. Dupilumab significantly improved the forced expiratory volume in 1 s, asthma control questionnaire score, the fraction of exhaled nitric oxide level, and immunoglobulin E level at 12 and 24 weeks (p < 0.05). However, it was associated with increased blood eosinophils at 12 and 24 weeks. Dupilumab was generally a safe agent for asthmatic patients. It showed no significant difference compared with the placebo regarding most adverse events. Conclusion: Dupilumab improves pulmonary function and reduces local and systemic inflammatory markers with minimal adverse events in patients with moderate to severe asthma.

Fenitrothion (FNT), a commonly used organophosphate, can cause oxidative damage and apoptosis on various organs. However, the underlying mechanisms for FNT-induced cardiotoxicity did not formally report. Here, we have evaluated the possible ameliorative roles of resveratrol (RSV) against FNT-induced cardiac apoptosis in male rats through the sirtuin1 (SIRT1)/c-Jun N-terminal kinase (c-JNK)/p53 pathway concerning pro-oxidant and inflammatory cytokines. Forty-eight male rats were equally grouped into control, RSV (20 mg/kg), 5-FNT (5 mg/kg), 10-FNT (10 mg/kg), 20-FNT (20 mg/kg), 5-FNT-RSV, 10-FNT-RSV, and 20-FNT-RSV where all doses administrated by gavage for four weeks. The present findings demonstrated that RSV markedly diminished the level of hyperlipidemia and elevation in lactate dehydrogenase (LDH), total creatine kinase (CK-T), and troponin T (TnT) levels following FNT intoxication. Furthermore, RSV significantly reduced FNT-induced cardiac oxidative injury by reducing malondialdehyde (MDA) level and improving the levels of glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and acetylcholinesterase (AchE). Also, the levels of interleukin-1β (IL1β,), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were significantly attenuated in the co-treated groups. Moreover, RSV alleviated the histopathological changes promoted by FNT and repaired the transcript levels of SIRT1, c-JNK, and caspase-9/3 along with p53 immunoreactivity. In silico study revealed that the free binding energies of RSV complexes with protein and DNA sequences of SIRT1 were lower than docked complexes of FNT. Therefore, RSV reserved myocardial injury-induced apoptosis following exposure to FNT by modulating the SIRT1/c-JNK/p53 pathway through cellular redox status and inflammatory response improvements.

Background & purpose: Exposure to organophosphorus during different phases of pregnancy induces many adverse impacts on the developing foetuses due to their immature detoxification system. We have estimated the potential amelioration role of quercetin against hepatic injury-induced apoptosis in rat foetuses following gestational exposure to fenitrothion and probable involvement of paraoxonase-1. Methods: Forty pregnant rats were allocated into four groups; the first one kept as control, the second intubated with quercetin (100 mg/kg), the third orally administrated fenitrothion (4.62 mg/kg) and the last group received quercetin two hours before fenitrothion intoxication. Results: Fenitrothion significantly elevated the foetal hepatic levels of thiobarbituric acid reactive substances, protein carbonyl, and nitric oxide, but it reduced the enzymatic activities of glutathione-S-transferase, superoxide dismutase, catalase, and acetylcholinesterase. Furthermore, fenitrothion provoked many histopathological changes in the foetal liver and markedly up-regulated the mRNA gene expression of p53, caspase-9 along with elevation in the immunoreactivity of Bax and caspase-3, but it down-regulated the expression level of paraoxonase-1. Remarkably, quercetin co-treatment successfully ameliorated the hepatic oxidative injury and apoptosis prompted by fenitrothion. Conclusions: Dietary supplements with quercetin can be used to reduce the risk from organophosphorus exposure probably through paraoxonase-1 up-regulation and enhancement of the cellular antioxidant system.

Ethoprophos, a common organophosphate nematicide, has adverse effects on the nervous system. However, the spe-cific mechanism of its neurotoxicity is unclear. Here, we have studied the possible involvement of brain glial fibrillary acidic protein and tubulin-associated unit in the neurotoxicity mechanism of ethoprophos, even at the threshold in-hibition of acetylcholinesterase. The adult male rats were divided into four groups (n = 8/group), including the con-trol and exposed groups that were orally received ethoprophos at the low (0.56 mg/kg), median (1.12 mg/kg), and high doses (2.24 mg/kg) for 90 days. Sub-chronic exposure to ethoprophos exhibited a significant decline in the brain activity and mRNA gene expression of acetylcholinesterase, while the levels of dopamine and serotonin were markedly increased at the medium and high doses (p < 0.01). Ethoprophos increased the anxiety-like behavior in rats subjected to the open field quiz and induced many histopathological alterations in the brain. Furthermore, ethoprophos markedly (p < 0.05) increased malondialdehyde and nitric oxide levels, while the glutathione content, together with the activities of glutathione peroxidase, glutathione-S-transferase, superoxide dismutase, and catalase were decreased in a dose-dependent manner. Additionally, there was a dose-dependent up-regulation in the mRNA gene expression of brain glial fibrillary acidic protein and tubulin-associated unit in the ethoprophos-exposed rats (p < 0.05). The obtained data deliver the initial demonstration about the involvement of this up-regulation in the neu-rotoxicity mechanism of ethoprophos and may use as a biomarker for organophosphate-induced neurodegeneration. (C) 2021 Elsevier B.V. All rights reserved.

Abamectin, an avermectin member, can induce significant neurodegeneration symptoms in non-target organisms. However, its neurodevelopmental influences in mammals are unclear. Here, we focus on the antiapoptotic action of alpha-mangostin against the developmental neurotoxicity of abamectin with the possible involvement of reelin and nestin mRNA gene expression. Thirty-two pregnant rats were allocated to four groups (8 rats/group); control, alpha-mangostin (20 mg/kg/d), abamectin (0.5 mg/kg), and co-treated group (alpha-mangostin + abamectin). The animals have gavaged their doses during the gestation period. The fetotoxicity and many signs of growth retardation were observed in the abamectin-intoxicated rats. In comparison with the control group, abamectin prompted a significant elevation (p < 0.05) in the levels of malondialdehyde and nitric oxide, along with many symptoms of histopathological changes in the fetal cerebral cortex. However, the glutathione, dopamine, and serotonin concentrations together with the activities of glutathione-S-transferase, catalase, and superoxide dismutase were markedly decreased (p < 0.05) in the abamectin group. Moreover, abamectin remarkably upregulated (p < 0.05) the brain mRNA gene expression of reelin, nestin, and caspase-9 as well as the immunoreactivity of Bax and caspase-3 proteins in the cerebral cortex. It should be noted that alpha-mangostin mitigated the developmental neurotoxicity of abamectin to the normal range by recovering the levels of oxidant/antioxidant biomarkers, catecholamines; and apoptosis-related proteins with the involvement of reelin and nestin genes regulation. Those records revealed that the transcription regulation of reelin and nestin could be involved in the neuroprotective efficacy of alpha-mangostin, especially avermectin's developmental neurotoxicity.

The association between gestational exposure to organophosphate and neurodevelopmental deficits is an area of particular interest, since the developing brain is sensitively susceptible to this neurotoxic pesticide. Instead, the neuroprotective role of quercetin has been suggested, but its exact protective mechanism against the developmental neurotoxicity of organophosphate did not previously notify. In this study, we have evaluated the anti-apoptotic role of quercetin against the developmental neurotoxicity of fenitrothion. Forty timed pregnant rats (from the 5th to the 19th day) were divided into four groups: control, quercetin (100 mg/kg/day), fenitrothion (2.31 mg/kg/day), and quercetin-fenitrothion co-treated groups where all animals received the corresponding doses by gavage. The embryotoxicity and many symptoms of the fetal growth retardation were recorded in the fenitrothion-intoxicated group. As compared with the control, fenitrothion brought significant (p < 0.05) elevation in the fetal brain dopamine, serotonin, and malondialdehyde levels as well as the activities of superoxide dismutase and catalase. However, fenitrothion decreased the glutathione concentration together with the activities of acetylcholinesterase, glutathione-S-transferase, and glutathione reductase. Moreover, fenitrothion induced some of the histopathological alterations in fetal brain and remarkably (p < 0.05) upregulated the mRNA gene expression of Bax and caspase-3 plus their protein immunoreactivity. It is worth mentioning that quercetin co-treatment alleviated (p ˂ 0.05) the fetal growth shortfalls, neurotransmission disturbances, lipid peroxidation, antioxidant disorders, and apoptosis evoked by fenitrothion with frequent repair to the control range. These results revealed that the downregulation of apoptosis-related genes and catecholamines is an acceptable indicator for the neuroprotective efficiency of quercetin especially during gestational exposure to organophosphate.

Supplementation with flavonoids plays a distinctive role in the protection against various chemicals as it has several health benefits. Nano-rich diesel exhaust particles (NRDEPs) contain more harmful chemical agents which have mutagenic, carcinogenic and/or teratogenic effects. So, the present study aims to evaluate the protective roles of quercetin against embryotoxicity of NRDEPs in albino rat fetuses. NRDEPs were characterized by transmission electron microscope, inductively coupled plasma atomic emission spectrometry and energy-dispersive X-ray spectrum. Forty pregnant rats were divided into four groups (10/each), first (control) group which received normal saline, dams of the second group received 100 mg/kg of quercetin, the third group received 20 mg/kg of NRDEPs and the fourth group received 100 mg/kg of quercetin two hours before NRDEPs exposure. All dams received their corresponding doses during the gestation period. The dams were undergone caesarean section at the end of gestation and their fetuses were removed from the uterus and evaluated for mortality rate, growth parameters, morphological and skeletal malformations together with histological study of placenta, brain and liver. The chemical analysis of NRDEPs revealed the presence of nanoparticles (30 to 60 nm), carbon nanotubes and a wide range of heavy metals as Al, Fe, Mn, Cu, Pb, Zn, Cr, V, Ba and Ni. Our results indicated that quercetin reduces the mortality rate, alleviates the growth retardation and suppresses the placenta, brain and liver histological lesions induced NRDEPs. In conclusion, quercetin may be useful in combating embryotoxic effects and tissue injury caused by NRDEPs without side effects.

The use of the older generation antiepileptic drugs (AEDs) during pregnancy and lactation is known to be associated with increased risk of birth defects in the offspring. Much less has been known about newer generation AEDs to which Levetiracetam (LEV) belongs. LEV is a broad spectrum antiepileptic drug which is currently licensed worldwide. The aim of this study was to evaluate the teratogenic effects of LEV on fetuses of albino rats. Pregnant albino rats(Rattusnorvegicus) were administered daily oral doses of 300mg/kg or 600mg/kg from the 5th day of gestation till the end of lactation. The animals were sacrificed at the end of gestation and during lactation. Fetuses were removed from the uterus and evaluated for mortality rate, growth parameters, morphological and skeletal malformations as well as histological study of brain, liver and kidney. The data revealed that fetal weights were significantly reduced in most study groups. Resorption rates were significantly increased with increasing LEV doses. It was found that mild degenerative changes were observed in the liver, kidney as well as the brain following LEV administration. Levetiracetam pretreatment caused a non-significant effect on the level of lipid peroxidation. No significant correlation was noted between GSH levels and the anticonvulsant effects of Levetiracetam. Thus administration of LVE during pregnancy and lactation should only be considered if the expected benefit to the mother is greater than any possible risk to the fetus.