Exogenous monosodium glutamate exacerbates lipopolysaccharide-induced neurobehavioral deficits, oxidative damage, neuroinflammation, and cholinergic dysfunction in rat brain.

Extensive experimental evidence points to neuroinflammation and oxidative stress as major pathogenic events that initiate and drive the neurodegenerative process. Monosodium glutamate (MSG) is a widely used food additive in processed foods known for its umami taste-enhancing properties. However, concerns about its potential adverse effects on the brain have been raised. Thus, the present study investigated the impact of MSG on lipopolysaccharide (LPS)-induced neurotoxicity in rat brains. Wistar rats weighing between 180 g and 200 g were randomly allocated into four groups: control (received distilled water), MSG (received 1.5 g/kg/day), LPS (received 250 µg/kg/day), and LPS + MSG (received LPS, 250 µg/kg, and MSG, 1.5 g/kg). LPS was administered intraperitoneally for 7 days while MSG was administered orally for 14 days. Our results showed that MSG exacerbated LPS-induced impairment in locomotor and exploratory activities in rats. Similarly, MSG exacerbated LPS-induced oxidative stress as evidenced by increased levels of malondialdehyde (MDA) with a concomitant decrease in levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione-s-transferase (GST) in the brain tissue. In addition, MSG potentiated LPS-induced neuroinflammation, as indicated by increased levels of pro-inflammatory cytokines such as interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) as well as myeloperoxidase (MPO) and nitric oxide (NO) in the brain. Moreover, MSG aggravated LPS-induced cholinergic dysfunction, as demonstrated by increased activity of acetylcholinesterase (AChE) in the brain. Further, we found a large number of degenerative neurons widespread in hippocampal CA1, CA3 regions, cerebellum, and cortex according to H&E staining. Taken together, our findings suggest that MSG aggravates LPS-induced neurobehavioral deficits, oxidative stress, neuroinflammation, cholinergic dysfunction, and neurodegeneration in rat brains.

Immuno-Kachiks formula immunomodulates and ameliorates hepatic damage induced by monosodium glutamate in rats.

The immune system plays a vital role in controlling liver fibrosis and enhancing the pathogenesis of liver inflammation. Monosodium glutamate is a common flavor-enhancement food additive. This study evaluated the immunomodulatory and hepato-curative effects of the Immuno-Kachiks polyherbal formulation against monosodium glutamate-induced immune suppression and hepatic damage in rats. Monosodium glutamate was given orally at a 2000 mg/kg dose to male Wistar rats for three months to induce liver damage and immune suppression. After three months of successful induction, three groups were separately administered orally with Immuno-Kachiks formula at 400, 800, and 1500 mg/kg/day for 28 days. At the end of the treatment period, liver and blood samples were collected for histological and biochemical analysis. The lymphocyte count remained significantly low while the neutrophil count and the neutrophil-to-lymphocyte ratio increased significantly, despite the cessation of monosodium glutamate ingestion for 28 days. The Immuno-Kachiks formula (IKF) significantly increased the lymphocyte count, reduced the neutrophil-to-lymphocyte ratio, and normalized the neutrophil count. Neither monosodium glutamate nor the IKF significantly caused alpha-fetoprotein levels to rise or fall below normal. High doses (800 and 1500 mg/kg) of the Immuno-Kachiks formula significantly raised serum levels of aspartate aminotransferase, alkaline phosphatase, and total bilirubin. 1500 mg/kg of the IKF caused mild liver inflammation. The IKF restored the liver morphologic alterations observed in monosodium glutamate-induced liver damage in rats. The results suggest that the Immuno-Kachiks herbal formulation is a potential curative agent for early-stage liver damage and could restore suppressed adaptive immunity.

Hematological changes, oxidative stress assessment, and dysregulation of aquaporin-3 channel, prolactin, and oxytocin receptors in kidneys of lactating Wistar rats treated with monosodium glutamate.

High consumption of locally produced delicacies could expose nursing mothers to high monosodium glutamate (MSG) levels, frequently used as a necessary condiment in low-income countries. Thus, this study evaluated some novel preliminary changes in renal hormonal receptors, the aquaporin-3 channel, oxidative stress markers, and hematological indices induced by monosodium glutamate in lactating rats. Post-parturition, twenty-four (24) lactating Wistar rats were divided into four (4) groups of six rats each (n = 6). Oral administration of distilled water and MSG started three (3) days postpartum as follows: group 1: distilled water (1 ml/kg BW), group 2: MSG (925 mg/kg BW), group 3: MSG (1850 mg/kg BW), and group 4: MSG (3700 mg/kg BW). At the end of the experiment, which lasted fourteen (14) days, animals were sacrificed and samples of blood and tissues were obtained for biochemical analysis. MSG administration significantly (p < 0.05) increased ROS and MDA, with a significant (p < 0.05) decrease in kidney antioxidants. Serum creatinine, total, conjugated, and unconjugated bilirubin significantly (p < 0.05) increased with MSG administration. The prolactin receptor was significantly reduced (p < 0.05), while the oxytocin receptor and aquaporin-3 channel were significantly (p < 0.05) increased in the MSG-administered groups. There were significant (p < 0.05) changes in the hematological indices of the MSG-administered animals. Thus, the findings of this study suggest that high MSG consumption causes hematological alterations and may alter renal function via increased ROS production and dysregulation of the AQP-3 channel, prolactin, and oxytocin receptors in the kidneys of lactating Wistar rats.

A Case of Type I Food Allergy Induced by Monosodium Glutamate.

Monosodium glutamate (MSG), a salt form of a non-essential amino acid, is widely used as a food additive, particularly in Asian cuisines, due to its unique flavor-enhancing qualities. Type I allergic reactions to MSG have not previously been reported. Our patient, a 21-year-old woman, was 14 years old when she first noticed swelling of her tongue (but no oral itching, diarrhea, or abdominal pain) after eating various snack foods. Current skin prick testing elicited a weak positive reaction to MSG. We then performed an oral challenge test during which our patient ingested potato snacks. Subsequent histology showed telangiectasia of the buccal mucosa, interstitial edema in the subepithelial submucosa, and mast cell infiltration. Oral mucosal challenge tests using sodium glutamate confirmed oral swelling in this patient. This report is the first to confirm a case of type 1 allergy to MSG by combining pathology findings with the results of challenge testing.

Unraveling the effects of drying techniques on chaya leaves: Metabolomics analysis of nonvolatile and volatile metabolites, umami taste, and antioxidant capacity.

Chaya (Cnidoscolus chayamansa) leaves are known for their strong umami taste and widespread use as a dried seasoning. This study aimed to assess the impact of different drying methods [freeze drying (FD), vacuum drying, oven drying at 50 °C and 120 °C (OD120) and pan roasting (PR)] on the metabolome using mass spectrometry, umami intensity, and antioxidant properties of chaya leaves. The predominant volatile compound among all samples, 3-methylbutanal, exhibited the highest relative odor activity value (rOAV), imparting a malt-like odor, while hexanal (green grass-like odor) and 2-methylbutanal (coffee-like odor) are the second highest rOAV in the FD and PR samples, respectively. OD120 and PR samples possessed the highest levels of umami-tasting amino acids and 5'-ribonucleotides as well as the most intense umami taste, whereas FD samples exhibited the highest antioxidant capacity. These findings enhance our understanding of the aroma characteristics, umami taste, and antioxidant potential of processed chaya leaves.

Unlocking Nature's Toolbox: glutamate-inducible recombinant protein production from the Komagatella phaffii PEPCK promoter.

BACKGROUND: Komagataella phaffii (a.k.a. Pichia pastoris) harbors a glutamate utilization pathway in which synthesis of glutamate dehydrogenase 2 and phosphoenolpyruvate carboxykinase (PEPCK) is induced by glutamate. Glutamate-inducible synthesis of these enzymes is regulated by Rtg1p, a cytosolic, basic helix-loop-helix protein. Here, we report food-grade monosodium glutamate (MSG)-inducible recombinant protein production from K. phaffii PEPCK promoter (PPEPCK) using green fluorescent protein (GFP) and receptor binding domain of SARS-CoV-2 virus (RBD) as model proteins. RESULTS: PPEPCK-RBD/GFP expression cassette was integrated at two different sites in the genome to improve recombinant protein yield from PPEPCK. The traditional, methanol-inducible alcohol oxidase 1 promoter (PAOX1) was used as the benchmark. Initial studies carried out with MSG as the inducer resulted in low recombinant protein yield. A new strategy employing MSG/ethanol mixed feeding improved biomass generation as well as recombinant protein yield. Cell density of 100-120 A600 units/ml was achieved after 72 h of induction in shake flask cultivations, resulting in recombinant protein yield from PPEPCK that is comparable or even higher than that from PAOX1. CONCLUSIONS: We have designed an induction medium for recombinant protein production from K. phaffii PPEPCK in shake flask cultivations. It consists of 1.0% yeast extract, 2.0% peptone, 0.17% yeast nitrogen base with ammonium sulfate, 100 mM potassium phosphate (pH 6.0), 0.4 mg/L biotin, 2.0% MSG, and 2% ethanol. Substitution of ammonium sulphate with 0.5% urea is optional. Carbon source was replenished every 24 h during 72 h induction period. Under these conditions, GFP and RBD yields from PPEPCK equaled and even surpassed those from PAOX1. Compared to the traditional methanol-inducible expression system, the inducers of glutamate-inducible expression system are non-toxic and their metabolism does not generate toxic metabolites such as formaldehyde and hydrogen peroxide. This study sets the stage for MSG-inducible, industrial scale recombinant protein production from K. phaffii PPEPCK in bioreactors.

Protective effect of Danshensu against neurotoxicity induced by monosodium glutamate in adult mice and their offspring.

Excessive neuronal excitation by glutamate is a well-established cause of neurotoxicity, leading to severe impairment of brain function. Excitotoxicity is a key factor in numerous neurodegenerative conditions. In this study, we investigated the neuroprotective effects of Danshensu (DSS) against monosodium glutamate (MSG)-induced neurotoxicity in adult mice and their offspring. We randomly divided one hundred 8-week-old Kunming mice (equal number of males and females) into a control group and an experimental group. The experimental group was further subdivided into various treatment groups, including MSG gavage treatment, bwbw DSS treatment group 1 (bwbw DSS treatment group 2, a drug control group, and a normal control group (receiving an equal volume of physiological saline for ten consecutive days). Additionally, another one hundred healthy 8-week-old Kunming mice were similarly divided into groups and treated. These mice were paired randomly (one male and one female) and pregnant females were housed separately to obtain offspring. Subsequently, we conducted histological and behavioral analyses on adult mice and their offspring. MSG treatment induced significant cellular edema and hippocampal damage in both the treated mice and their offspring. However, varying doses of DSS effectively counteracted the neurotoxic effects of MSG, with no adverse impact on brain tissue structure or neural function in either adult mice or their offspring. Behavioral experiments further confirmed that DSS exerted a substantial protective effect against MSG-induced impairment of learning and memory in the treated adult mice and their offspring, in addition to mitigating central nervous system overexcitation and inhibiting exploratory behavior. In conclusion, DSS exerts significant protective effects against MSG-induced neurotoxicity in both adult mice and their offspring.

Quercetin inhibits NF-kB and JAK/STAT signaling via modulating TLR in thymocytes and splenocytes during MSG-induced immunotoxicity: an in vitro approach.

BACKGROUND: The most widely used food additive monosodium glutamate (MSG) has been linked to immunopathology. Conversely, quercetin (Q), a naturally occurring flavonoid has been demonstrated to have immunomodulatory functions. Therefore, the purpose of the study is to determine if quercetin can mitigate the deleterious effects of MSG on immune cells, and the possible involvement of TLR, if any.  METHODS AND RESULTS: This study was conducted on Q, to determine how it affects the inflammatory response triggered by MSG in primary cultured thymocytes and splenocytes from rats (n = 5). Q shielded cells by augmenting cell survival and decreasing lactate dehydrogenase leakage during MSG treatment. It decreased IL-1ß, IL-6, IL-8, and TNF-α expression and release by hindering NF-kB activation and by inhibiting the JAK/STAT pathway. Moreover, Q prevented NLRP3 activation, lowered IL-1ß production, and promoted an anti-inflammatory response by increasing IL-10 production. Q reduced MSG-induced cellular stress and inflammation by acting as an agonist for PPAR-γ and LXRα, preventing NF-kB activation, and lowering MMP-9 production via increasing TIMP-1. Additionally, Q neutralized free radicals, elevated intracellular antioxidants, and impeded RIPK3, which is involved in inflammation induced by oxidative stress, TNF-α, and TLR agonists in MSG-treated cells. Furthermore, it also modulated TYK2 and the JAK/STAT pathway, which exhibited an anti-inflammatory effect. CONCLUSIONS: MSG exposure is associated with immune cell dysfunction, inflammation, and oxidative stress, and Q modulates TLR to inhibit NF-kB and JAK/STAT pathways, providing therapeutic potential. Further research is warranted to understand Q's downstream effects and explore its potential clinical applications in inflammation.

Quercetin counteracts monosodium glutamate to mitigate immunosuppression in the thymus and spleen via redox-guided cellular signaling.

BACKGROUND: Chronic inflammation brought on by oxidative stress can result in several immunopathologies. Natural compounds with antioxidant characteristics, like quercetin, have shown effectiveness in reducing oxidative damage and regulating the immune response. PURPOSE: The commonly used food additive monosodium glutamate (M) causes immunosuppression by disrupting redox equilibrium and inducing oxidative stress. The goal of this work is to examine the therapeutic potential of quercetin against immunotoxicity brought on by M, revealing the molecular route implicated in such immunopathology by targeting the thymus and spleen, to support the development of future anti-inflammatory and antioxidant therapies. STUDY DESIGN AND METHODS: M-fed rats were employed as an immunotoxicity model and were supplemented with quercetin for four weeks. Hematological and biochemical parameters were measured; H&E staining, immunohistochemistry, flow cytometry, real-time quantitative PCR, and western blotting were performed. RESULTS: Based on the findings, TLR4 was activated by M to cause oxidative stress-mediated inflammation, which was alleviated by the supplementation of quercetin by modulating redox homeostasis to neutralize free radicals and suppress the inflammatory response. To prevent M-induced inflammation, quercetin demonstrated anti-inflammatory functions by blocking NF-kB activation, lowering the production of pro-inflammatory cytokines, and increasing the release of anti-inflammatory cytokines. By normalizing lipid profiles and lowering the potential risk of immunological deficiency caused by M, quercetin also improves lipid metabolism. Additionally, it has shown potential for modifying insulin levels, suggesting a possible function in controlling M-induced alteration in glucose metabolism. The addition of quercetin to M enhanced the immune response by improving immunoglobulin levels and CD4/CD8 expression in the thymus and spleen. Additionally, quercetin inhibited apoptosis by controlling mitochondrial caspase-mediated cellular signaling, suggesting that it may be able to halt cell death in M-fed rats. CONCLUSION: The results of this study first indicate that quercetin, via modulating redox-guided cellular signaling, has a promising role in reducing immune disturbances. This study illuminates the potential of quercetin as a safe, natural remedy for immunopathology caused by M, including thymic hypoplasia and/or splenomegaly, and paves the way for future anti-inflammatory and antioxidant supplements.

Monosodium Glutamate Even at Low Dose May Affect Oxidative Stress, Inflammation and Neurodegeneration in Rats.

Monosodium glutamate (MSG) is a widely used flavour enhancer. A daily intake of MSG at high dosage (2000-4000 mg/kg body weight) is reported to be toxic to humans and experimental animals. The present study aims to investigate the toxic effect of oral administration of MSG at low concentrations (30 and 100 mg/kg body weight) by evaluating biochemical parameters of oxidative stress and inflammation in blood; expression of neuroinflammatory gene and histopathological changes in brain on male Wistar rats. The administration of MSG significantly increases serum level of fasting glucose, insulin, triglycerides, total cholesterol, low-density lipoprotein and decrease level of high-density lipoprotein. Significant low level of FRAP, GSH, SOD, CAT and higher level of MDA, PCO, AOPP, PMRS, NO, CRP, IL-6, TNF-α confirms substantial oxidative stress followed by inflammation after 100 mg MSG treatment. RT-PCR figure shows significant expression of neuroinflammatory gene IL-6 and TNF-α and histopathological examination revealed severe neurodegeneration in hippocampus (CA1 and CA3) and cerebral cortex region of brain at 100 mg MSG treatment. Our result provides evidence that MSG administration at 30 mg does not impose toxicity, however at 100 mg/kg body weight, which is considered a low dose, there is significant toxic effects and may be detrimental to health.

Immune boosting and ameliorative properties of aqueous extract of Vernonia amygdalina Delile against MSG-induced genotoxicity: An in silico and in vivo approach.

Vernonia amygdalina (VA) is popularly consumed as food and as medicine due to its nutritional and bioactive constituents. This study assessed the anti-genotoxic effect of aqueous leaf extract of VA against monosodium (MSG) -induced genotoxicity. Crude extraction and phytochemical analysis were done using standard methods. In silico studies was done using compounds in the extract against Bcl-2, NF-kB 50, DNA polymerase lambda, DNA ligase, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX). Twelve rats were divided into three groups with four rats in each group. Group I was fed on food and water, group II received MSG (4 g/kg) per body weight (pbw) intraperitoneally, group III received MSG (4 g/kg) pbw intraperitoneally followed by oral dose of VA leaf extract (250 mg/kg) per body weight. The number of the micronucleated red blood cells and white blood cells were determined from blood smears microscopically. Results showed that aqueous extract of VA contained in mg/100 g alkaloids (7.04 ± 0.16), saponins (3.91 ± 0.13), flavonoid (1.64 ± 0.16), phenol (3.40 ± 0.12) and tannins (0.07 ± 0.32). In silico studies revealed high binding interaction (ΔG > -8.6) of vernoniosides D and E with all the tested proteins. There was a reduction in the number of micronucleated cells, neutrophils and eosinophils of the treated group compared to the MSG group, while there was an increase in the lymphocyte count. The anti-genotoxic effects of VA leaf extract might be attributed to the synergistic interaction of the various bioactive components in the extract. VA could be a potential plant for the prevention of cancer and other diseases that attenuate the immune system.

Disruptive consequences of monosodium glutamate on male reproductive function: A review.

Monosodium glutamate (MSG) is one of the most extensively used flavour enhancers worldwide. Although it is widely regarded as a safe food additive with no recommended daily dosage, its over-consumption has been associated with notably pathophysiological events in various tissues and organs of the body. Previous studies have reported of the neuro- cardio- and hepato- toxic effects of its excessive exposure. Moreover, the food additive instigates metabolic dysfunction. It has been established that MSG damages male reproductive accessory organs like prostate glands and epididymis. In addition, it impairs serum enzymatic activities and serum levels of testosterone, gonadotropin-releasing hormone, luteinizing hormone and cholesterol. Reduced sperm count, sperm motility, sperm morphology, and sperm viability, imbalances in male reproductive hormones, alongside alteration in the histoarchitecture of the testes and other male reproductive tissues have also been connected with excessive exposure to MSG. Literature reports affirm the link between the over-consumption of MSG and reproductive organ weight and male sexual behaviour. This review article addresses the multi-systemic effects of exposure to MSG and the possible mechanism of action of the compound with a focus on the negative implications of the food additive on male reproductive functions and the possible role of natural antioxidants in male reproductive functions. carefully selected keywords were used during the literature search to gather credible and up-to-date information about the subject matter.

Investigating the effect of exposure to monosodium glutamate during pregnancy on development of autism in male rat offspring.

In present study, we investigated the relationship between the pregnancy exposure to monosodium glutamate (MSG) and autism development in male offspring of rats. Pregnant Wistar rats were allocated into five groups. The first group was control group that pregnant animals received normal saline orally from day 1-18 of pregnancy. Group 2, 3 and 4 pregnant rats received different doses (1.5, 5 and 10 g/kg) of MSG by the same way respectively. Group 5 received 500 mg/kg of Valproic acid (VPA) on the 12.5th day of pregnancy. Different behavioral tests including marble burying, self-grooming, and Barnes maze test were performed on offspring. The levels of glutamate and GSH markers were also measured. The results showed that MSG similar to VPA led to induction of autistic anxiety and repetitive behaviors. It could also deteriorate the spatial memory. Besides we found that behavioral symptoms potentiated with increasing the MSG dosage. Similarly, we had an increase in glutamate and a reduction in GSH levels in offspring. Findings indicated that MSG was able to induce autism in offspring of rats in a dose-dependent way. This effect could be through increasing of glutamate and reduction of GSH. Consequently, MSG should be avoided during pregnancy.

Effects of vincristine and monosodium glutamate on gastrointestinal motility and visceral sensitivity.

BACKGROUND: Chemotherapy-induced adverse effects are an unresolved nightmare. In preclinical studies in rats, the food additive monosodium glutamate (MSG) improved some of the side effects caused by cisplatin, but its effects in other models of chemotherapy-treated animals are not well known. The aim of this study was to test if MSG may improve some of the adverse effects induced by vincristine in rats. METHODS: Young male Wistar rats were exposed or not to MSG (4 g L-1 ) in drinking water from week 0 till 1 week after treatment (week 3). Rats received two cycles of five daily intraperitoneal (ip) injections (Monday to Friday, weeks 1 and 2) of either saline (2 mL kg-1 ) or vincristine (0.1 mg kg-1 ). Gastrointestinal motility was measured in vivo by radiological methods after the first and tenth ip administrations. On week 3, the threshold for mechanical somatic and colorectal sensitivity was recorded using Von Frey filaments applied to the paws and an intracolonic balloon, respectively. Finally, samples of the terminal ileum and distal colon were histologically evaluated in sections. KEY RESULTS: Vincristine reduced body weight gain, food intake, and upper gastrointestinal transit, caused somatic (but not visceral) hypersensitivity and increased the thickness of the submucosal and muscle layers of the small intestine. In vincristine-treated animals, MSG partially prevented gastrointestinal dysmotility and reduced visceral sensitivity but did not improve structural alterations of the small intestine. CONCLUSIONS & INFERENCES: MSG could be used as an adjuvant to conventional treatments to improve some gastrointestinal dysfunctions caused by chemotherapy.

The investigation of the effects of monosodium glutamate on healthy rats and rats with STZ-induced diabetes.

Monosodium glutamate (MSG, E621) is a flavor-enhancing food additive used widely in the food preparation industry and consumed regularly. It is considered that long-term consumption of MSG causes metabolic syndrome and obesity. Diabetes mellitus (DM) is a chronic metabolic disease characterized by high blood sugar, polyuria, polydipsia, and polyphagia, in which insulin secreted from pancreatic ß cells is inadequate for maintaining blood glucose homeostasis. Rats were application 65 mg/kg streptozotocin (STZ) solution intraperitoneally and a diabetes model was created. For this purpose, freshly prepared STZ was injected into the peritoneum. Tumor necrosis factor-α, interleukin (IL)-10, IL-6, and IL-1ß levels in STZ, MSG, and STZ + MSG groups were found to be significantly increased in inflammation parameters measured on the 28th day of administration when compared to the Control Group (p < 0.001). Also, although malondialdehyde (MDA) levels increased significantly in the STZ + MSG group when compared to the control group (p < 0.001), glutathione (GSH), and superoxide dismutase (SOD) levels were significantly decreased in the STZ, MSG, and STZ + MSG groups when compared to the control group (p < 0.001). Also, although glucose levels increased significantly in STZ and STZ + MSG at the end of the 28th day (p < 0.01), insulin levels decreased in STZ, MSG, and STZ + MSG groups when compared to the control groups (p < 0.01). As a result, it was found that STZ and MSG application significantly increased cytokine production, increased MDA, which is an oxidant parameter in pancreatic tissue, and decreased antioxidants (GSH and SOD) when compared to the control groups. It was also found that MSG disrupted the normal histological structure in pancreatic cells, and the damage was much more in both exocrine and endocrine pancreatic areas in the STZ + MSG group when compared to the STZ and MSG groups. It was considered that with the increased use of MSG, the susceptibility to DM might increase along with tissue damage significantly in diabetic groups, therefore, MSG must be used in a limited and controlled manner.

Spice-Induced Metal Contamination and Microbiological Risk Assessment of Instant Noodles Prepared for Human Consumption.

With the rising worries of potential metal contamination in cooked noodles, this study aimed at unravelling, for the first time, the possible source of metal contamination in cooked noodles. Noodles cooked with full spices (CWFS), cooked with half spices (CWHS), cooked with quarter spices (CWQS), and cooked with no spices (CWNS: control) and their spices were analysed for metals using inductively coupled plasma-atomic emission spectrometry. The microbiological quality of the noodles was also evaluated. Metal concentrations in cooked noodles varied with spice quantity. Noodles CWFS had the highest significant (p < 0.05) concentration of Pb (0.36 ± 0.12 mg/kg), Ni (1.05 ± 0.01 mg/kg), Cd (0.07 ± 0.04 mg/kg), Co (0.02 ± 0.002 mg/kg), and Na (9.45 ± 0.04 mg/kg), compared to the control (CWNS). The mean Pb and Ni of spice and cooked noodles were above the WHO acceptable limits for food and could be harmful to consumers. Pearson's correlation and PCA showed that packed noodle spices introduced metals into the cooked noodles. Although the hazard indices (adults and children) in all noodle's groups were less than 1, children still had the potential to contract cancer from Ni exposure because the carcinogenic risk values of CWQS (2.87 × 10-4), CWHS (3.03 × 10-4), and CWFS (3.21 × 10-4) were greater than 10-4. Microbiological analysis revealed the presence of potential pathogens that showed multidrug resistance and the ability to elaborate protease and amylase enzymes. Given the impending chronic health risks inherent in processed noodles, consistent consumption should be avoided.

HISTOLOGICAL AND MORPHOLOGICAL CHANGES IN THE LYMPHOID STRUCTURES OF THE GASTRIC MUCOUS MEMBRANE IN WHITE RATS WITH THE ADMINISTRATION OF SODIUM GLUTAMATE.

OBJECTIVE: The aim: To determine the histological and morphological changes of the lymphoid structures of the stomach in male rats under the influence of oral sodium glutamate at the rate of 15 mg/kg of body weight. PATIENTS AND METHODS: Materials and methods: The scientific experiment was performed on 20 white non-linear male rats of reproductive age (4-5 months). The experimental animals were divided into two groups (10 rats in each group), which were orally received monosodium glutamate at a dose of 15 mg/kg body weight every day. We studied the effect of 2 and 4 weekly administration of monosodium glutamate at a dose of 15 mg/kg body weight, respectively, in the I and II groups of experimental animals (depending on the week of their decapitation). Rats of the control groups (n=10) were injected with a placebo for 2 and 4 weeks, namely 0.5 ml of dechlorinated tap water at room temperature. Intact control animals were also divided into two groups, 5 rats each, depending on the week of decapitation: respectively, III group - decapitation on the 2nd week of the experiment; IV group - decapitation on the 4th week of the experiment. After the experiments were completed, animals were decapitated under light ether anesthesia. According to the purpose of the study, pieces of rat stomach measuring 1.0 x 1.0 cm were taken from the front wall of the bottom of the stomach near the great curvature, cardiac and portal parts of the organ. Histological preparations were examined using a MICROmed SEO SСAN light microscope and a Vision CCD Camera. Morphometric studies were carried out according to the method of S. B. Stefanov, using grids No. 3/16. For electron microscopic examination, pieces of the stomach wall of rats were fixed in a 2.5% solution of glutaraldehyde in a 0.1 M phosphate buffer (pH 7.2-7.4) with subsequent fixation in a 2.0% solution of osmium tetroxide. After dehydration in alcohols and acetone, the material was embedded in eponaraldite. Sections were made on an LKB-8800-III ultramicrotome and studied using a JEM - 100-V microscope. To study the structural components of the lymphoid formations of the mucous membrane of different parts of the stomach of rats, semi-thin sections were made for the purpose of sharpening the blocks, which were stained with methylene blue. RESULTS: Results: The analysis of the obtained data of the conducted experiment indicates that the administration of monosodium glutamate in a dose of 15 mg/kg of body weight to rats already after 14 days leads to an increase in the density and size of the lymphoid structures of the GMM. The number of immunocompetent cells between the fundus of the gastric glands and the muscle plate increases in the diffuse lymphoid tissue of the gastrointestinal tract of rats in all its parts, both in the I and II groups of experimental animals. These changes are most pronounced in the cardiac and portal parts of the stomach. In both groups of experimental animals, the migration of interepithelial lymphocytes, macrophages, plasma cells, and tissue basophils to the surface epithelium increases. In both groups of experimental animals (and the II group of rats), lymphoid nodules and lymphoid pre-nodules of the gastric mucous membrane (GMM) are located between the bottom of the gastric glands and the muscular plate of the GMM. A gradual increase of medium lymphocytes in the GMM was established both in animals of I and II groups, while large lymphocytes increased in almost the same amount in experimental animals of both groups. Similar changes occur in the characteristics of the number of plasma cells, macrophages and tissue basophils in the lymphoid pre-nodules of GMM. CONCLUSION: Conclusions: Administering monosodium glutamate to rats at a dose of 15 mg/kg of body weight for 2 weeks leads to an increase in the density and size of lymphoid structures of the mucous membrane in all parts of the stomach with a predominant increase in the number of immunocompetent cells between the bottom of the gastric glands and the muscle plate. At the same time, more pronounced changes were found in the number of small lymphocytes, which tend to decrease by the 2nd week of the experiment, and vice versa - their density increases by the 4th week of monosodium glutamate administration.

HISTOLOGICAL AND MORPHOLOGICAL CHANGES OF THE VASCULAR BED OF THE THYMUS IN WHITE RATS UNDER THE INFLUENCE OF MONOSODIUM GLUTAMATE.

OBJECTIVE: The aim: To evaluate the effect of 28-day oral administration of MSG at the rate of 30 mg/kg of body weight on histological and morphometric parameters of the vascular bed of the thymus in rats. PATIENTS AND METHODS: Materials and methods: The scientific experiment was conducted on 20 white non-linear rats of reproductive age (4-5 months) weighing from 220 to 280 g, which were divided into two groups (10 rats each). Depending on the term of decapitation, the experimental animals were divided into two groups (10 rats in each group). We studied the effect of 14 and 28 days of MSG administration on the body of rats (I and II groups of experimental rats). The experimental animals were daily orally treated with MSG at a dose of 30 mg/kg body weight, which was dissolved in 0.5 ml of dechlorinated tap water at room temperature. Control rats of III and IV groups (5 rats in each of the control groups) were injected with a placebo (0.5 ml of dechlorinated tap water at room temperature) for 14 and 28 days. Intact animals of III and IV groups were also decapitated on the 14th and 28th days of the experiment, respectively. After the end of the experiment, animals were decapitated under light ether anesthesia. After decapitation, the animals were dissected into the chest cavity to remove the thymus. Histological preparations were studied using a MICROmed SEO SСAN light microscope and a Vision CCD Camera. Morphometric studies were carried out using VideoTest-5.0, KAARA Image Base and Microsoft Excel programs on a personal computer. RESULTS: Results: During the microscopic examination of histological preparations of the retrosternal gland in experimental animals of the 1st group (daily administration of MSG at the rate of 30 mg/kg of body weight for 14 days), it was established that the lumen of the arteries is moderately filled with blood elements. The veins are dilated with a changed shape and filled with blood. The following ultrastructural changes were detected in the experimental animals of group I: the lumen of arteries, arterioles and venules is slightly expanded, the nuclei of endotheliocytes are enlarged, occupy a significant part of the cytoplasm, the karyolem forms intussusceptions. The plasmolemma of the lumenal surface of endotheliocytes forms numerous microvilli. At the same time, organelles in the cytoplasm of endotheliocytes lose their contours. After 28 days of exposure to MSG at a dose of 30 mg/kg of body weight in rats (II group of experimental animals), structural changes in the vascular bed of the thymus worsened. The wall of arteries and arterioles is more thickened and swollen, collagen fibers are stratified. In their lumen, there are many uniform elements attached to the vascular wall and testify to thrombus formation. Perivascular edema is determined. The diameter of hemocapillaries is increased, their basal membrane is swollen. Veins and venules are also dilated, full blood, interendothelial contacts in the vessel wall are dilated, the basement membrane is damaged. This contributes to the diapedesis of blood plasma through the vessel wall, which leads to perivascular edema. CONCLUSION: Conclusions: Administration of MGS to rats at a dose of 30 mg/kg of body weight for 14 days leads to violations of the morphometric indicators of the vascular bed in the thymus, namely, to an increase in the outer and inner diameter of the arteries, an increase in the area of the middle membrane and the lumen of the vessels, which tend to progress with maximum indicators on the 28th day of the experiment. 2. The study of the vascular bed of the thymus against the background of taking MSG in a dose of 30 mg/kg of the weight of rats indicates the most pronounced changes in hemocapillaries, mainly on the 28th day of the experiment, which is manifested by an increase in their outer diameter. In the lumen of the hemocapillaries, deformed erythrocytes are identified, arranged in the type of "coin columns".

A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer's disease-like animal model.

This systematic review analyzes monosodium glutamate (MSG) in the Alzheimer's disease-like condition to enhance translational research. Our review seeks to understand how MSG affects the brain and causes degenerative disorders. Due to significant preclinical data linking glutamate toxicity to Alzheimer's disease and the lack of a comprehensive review or meta-analysis, we initiated a study on MSG's potential link. We searched PubMed, ScienceDirect, ProQuest, DOAJ, and Scopus for animal research and English language papers without time constraints. This study used the PRISMA-P framework and PICO technique to collect population, intervention or exposure, comparison, and result data. It was registered in PROSPERO as CRD42022371502. MSG affected mice's exploratory behaviors and short-term working memory. The brain, hippocampus, and cerebellar tissue demonstrated neuronal injury-related histological and histomorphometric changes. A total of 70% of MSG-treated mice had poor nesting behavior. The treated mice also had more hyperphosphorylated tau protein in their cortical and hippocampus neurons. Glutamate and glutamine levels in the brain increased with MSG, and dose-dependent mixed horizontal locomotor, grooming, and anxiety responses reduced. MSG treatment significantly decreased phospho-CREB protein levels, supporting the idea that neurons were harmed, despite the increased CREB mRNA expression. High MSG doses drastically lower brain tissue and serum serotonin levels. In conclusion, MSG showed AD-like pathology, neuronal atrophy, and short-term memory impairment. Further research with a longer time span and deeper behavioral characterization is needed. Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier [CRD42022371502].

Investigating the Chemical Composition of Lepidium sativum Seeds and Their Ability to Safeguard against Monosodium Glutamate-Induced Hepatic Dysfunction.

Monosodium glutamate (MSG) is one of the most frequently used food additives that endanger public health. The antioxidant, hyperlipidemic, and cytoprotective properties of Lepidium sativum seeds (LSS) as a natural remedy can minimize the harmful effects of MSG. This study investigated the potential protective effect of LSS against MSG-induced hepatotoxicity in rats. Male albino Sprague Dawley rats (n = 24) were equally divided into four groups for 30 days: the control group (G1) received a basal diet without supplement, group (G2) was fed a basal diet + MSG (30 g/kg b.w.) as a model group, group (G3) was fed a basal diet + MSG (30 g/kg b.w.) + LSS (30 g/kg b.w.), and group (G4) was fed a basal diet + MSG (30 g/kg b.w.) + LSS (60 g/kg b.w.). LSS enhanced serum alkaline phosphatase activity as well as total cholesterol, triglyceride, and glucose levels. It can decrease peroxide content in serum lipids and inhibit glutathione reductase and superoxide dismutase in hepatic cells. The dietary supplementation with LSS provided cytoprotection by enhancing the histoarchitecture of the liver and decreasing the number of apoptotic cells. Due to their antioxidant and anti-apoptotic properties, LSS effectively protect against the hepatotoxicity of MSG. These findings are of the highest significance for drawing attention to incorporating LSS in our food industry and as a health treatment in traditional medicine to combat MSG-induced hepatic abnormalities.