Monosodium Glutamate Toxicity Research Articles

The Role of Vitamin C on ATPases Activities in Monosodium Glutamate-Induced Oxidative Stress in Rat Striatum and Cerebellum.

Monosodium glutamate (MSG) is a silent excitotoxin used as a flavour enhancer but exerts serious health hazards to consumers. MSG plays a role in neuronal function as the dominant excitatory neurotransmitter. It is transferred into the blood and ultimately increases brain glutamate levels, causing functional disruptions notably via oxidative stress. The study evaluated the toxic effect of high consumption of MSG and the modulatory role of vitamin C on ATPase activities in the striatum and cerebellum of male Wistar rats for five weeks. Rats were grouped into four (A-D): group A was fed with rat's show only; Group B was fed with diet containing 15% MSG; Group C was treated with vitamin C (200mg/kg b.wgt orally in 0.9% saline solution) only for 3weeks; and group D rats were fed with MSG and vitamin C. The findings show that MSG does not affect body and cerebellum weights but increases striatal weight. MSG increases the malondialdehyde (MDA) level and significantly decreases catalase (CAT) and superoxide dismutase (SOD) activities and glutathione (GSH) levels. MSG significantly impaired striatal and cerebellar ATPases activities (Na+/K+-, Ca2+-, Mg2+- and total ATPases). Vitamin C treatment abolishes MSG-induced oxidative stress and improves ATPase activities. The findings show that vitamin C has beneficial effects in improving the functions of membrane-bound ATPases against MSG toxicity in rat's striatum and cerebellum.

Histopathological alterations in the vital organs of Indian major carp Labeo rohita exposed to monosodium glutamate (MSG)

BackgroundMonosodium glutamate (MSG E621) is one of the most popular flavouring agents of modern times and is widely used in many commercially packed food and even in house hold cooking. Previous studies revealed that excessive intake of MSG in diet causes obesity, metabolic defects, nephrotoxicity, neurotoxicity and hepatotoxicity in rats, but no reports are available in the literature about the ecotoxicological assessment of MSG by using fishes as a bioindicators. Since fishes are important consumer in aquatic food chain and directly linked with human health status, the present study was aimed to investigate the impact of MSG in freshwater fish Labeo rohita by using histological biomarkers.ResultsNinety-six h-LC50 of MSG to Labeo rohita was determined (1.5 g/L), and fish exposed to sub-lethal concentration of MSG (1/10th of 96 h-LC50 concentration of MSG (150 mg/L)) showed distinguished behavioural changes like erratic movement, loss of appetite and excessive mucous secretion all over the body as an adaptive syndrome to avoid the direct exposure to MSG in the medium. Histopathological analysis clearly depicts severe damages in the vital organs of fish. In gills, epithelial necrosis, hypertrophy, hyperplasia, primary and secondary gill lamellae degeneration, oedema, fusion of adjacent secondary lamellae and rupture of gill epithelium were observed. The intensity of tissue damage was increased as the exposure period was extended. The liver displayed vein congestion, vacuole formation, degeneration in parenchymal cells and bile stagnation, whereas MSG-treated kidney tissue showed high interstitial inflammation. Among the vital organs gill and liver displayed the highest histopathological alterations.ConclusionsThe present study clearly demonstrated that MSG is toxic to fish and able to cause significant damages in the vital organs as the exposure period was extended. Since the studies on the toxicity of MSG to fish are rare, the present investigation may contribute to the scarce literature on sub-lethal toxicity of MSG to freshwater fishes.

Investigation of Potential Protective effects of Betanin on experimental Monosodium Glutamate–induced toxicity in Elderly rats

This study was conducted to investigate the protective effects of Betanin active ingredient in red beetroot plant (Beta vulgaris) in elderly rats exposed to chronic toxicity of monosodium glutamate (MSG). A total of 48 elderly rats were randomly divided into 4 different groups. At the end of the 28–day study, the rats were sacrificed under deep anesthesia. Total antioxidant capacity (TAC), total oxidant capacity (TOC), paraoxonase (PON), thiol, malondialdehyde (MDA), and nitric oxide (NO) levels were investigated in rat blood serum using the spectrophotometric method. Oxidative Stress Index (OSI) was calculated by dividing TOC by TAC. Total bilirubin was measured with the colorimetric method using an ELISA kit. Liver tissues were stained with hematoxylin–eosin (HE) for histopathological examination. The difference in serum levels of TAC, TOC, OSI, PON, MDA, and thiol was statistically significant between the groups (P<0.05). The difference in serum levels of NO and total bilirubin was not statistically significant between the groups (P>0.05). The analysis of histopathological findings revealed uncommon mild hydropic degeneration in the MSG group and almost normal histological appearance in the MSG+Betanin group. This study demonstrated that betanin could increase the antioxidant effect and reduce the histopathological damage caused by MSG.

Monosodium Glutamate Effect on The Expression of ɑ7nACHR and ɑ4nACHR Subunits in The Testicular Tissue.

Monosodium glutamate (MSG) is a popular food flavor enhancer, and a glutamate subset that induces different toxicities such as hepatotoxicity, neurotoxicity, reproductive toxicity, and nephrotoxicity. This study was conducted to assess the effects of MSG on the α7 and α4 nicotinic acetylcholine receptor (nACHR) protein subunits expression of adult rat testis and the safety role of vitamin C. For this experimental research, 24 rats were haphazardly grouped into four equal groups (n=6) and orally gavaged for 30 days as follows: control group (distilled water gavage), MSG group (3 g/kg/b.w/ day), vitamin C group (150 mg/kg/b.w/day), and MSG+vitamin C group (3 g/kg/b.w/day+150 mg/kg/b.w/day, respectively) that rats of all groups on the 30th day were anesthetized, and the left testes were used for of α4 and α7 nACHR protein subunit evaluation by immunohistochemistry (IHC). Statistical computations were performed using Graph Pad Prism software. The present study revealed a significant reduction in the expression and optical density (OD) of α7 nACHR and α4 nACHR in the seminiferous tubules and intertubular connective tissue in the MSG group compared to the control group. In the MSG+vitamin C group, the expression and OD of α7 nACHR and α4 nACHR increased in the seminiferous tubules and intertubular connective tissue but this improvement was not significant compared to the MSG group. MSG decreased the expression level of nACHR protein subunits, α7 and α4, in the seminiferous tubules and interstitial testicular tissue. Vitamin C in the MSG+vitamin C group could not significantly improve the expression of α7 and α4 nACHR subunits in testicular tissue. Probably, MSG toxicity can be compensated with higher doses of vitamin C.

Phoenix dactylifera and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats.

Monosodium glutamate (MSG) has been known to cause neurodegeneration, due to its ability to trigger excitotoxicity, and the hippocampus is one of the most affected regions. Therefore, Phoenix dactylifera (P. dactylifera) and polyphenols was employed in this study to mitigate on the deleterious effect of monosodium glutamate on the dentate gyrus of Wistar rats. Forty-eight male Wistar rats weighing between 120-150g was used for the study. The Wistar rats were grouped into eight, (n=6). Groups 1-8 received 1.6mL/kg normal saline, 4000mg\kg monosodium glutamate for 7-days, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg caffeic-acid for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg Phoenix dactylifera for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days concurrently, 100mg\kg. caffeic-acid for 14-days followed by 4000mg\kg monosodium glutamate for 7-days, 100mg\kg Phoenix dactylifera for 14-days followed by 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days followed by 4000mg\kg monosodium glutamate for 7-days respectively. After the treatments, the rats underwent behavioural tests, and subsequently, the brain tissues were processed for histological and biochemical analyses. The activities of P. dactylifera and polyphenols ameliorated the deleterious effect of monosodium glutamate, through increased spontaneous alternation of the experimental animals, dominant matured granule cells of the dentate gyrus and modulated the activities of superoxide dismutase, glutathione peroxidase and malondialdehyde in the of male Wistar rats. Therefore, this study revealed that P. dactylifera and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats.

Testicular Effect of Selenium Nanoparticles on Monosodium Glutamate Induced Alteration in Male Albino Rats.

<b>Background and Objective:</b> The flavor enhancer Monosodium Glutamate (MSG) is mostly utilized in Asian and West African cuisines, especially in West African and Asian dishes. However, due to its availability, largely without labeling, in many food products, unintentional overuse of this food additive may occur. The objective of this study was to find out how selenium nanoparticles affected the toxicity of MSG in male albino rats' testicles. <b>Materials and Methods:</b> As 35 Wistar male rats partitioned into 5 groups: G1: Control rats, G2: Received Se-NPs at 0.4 mg kg<sup>1</sup> b.wt., orally, G3: Injected with MSG at a daily dose of 4 g kg<sup>1</sup> b.wt., intraperitoneally (IP), G4: Ingested a daily oral dose of Se-NPs for 7 successive days and on the 7th day, received the first dose of MSG IP 4 g kg<sup>1</sup> b.wt., then received both treatments till the end of the study and G5: Administered a daily oral dose of 4 g kg<sup>1</sup> MSG, followed by Se-NPs at a daily dose of 0.4 mg kg<sup>1</sup> b.wt., the experiment continued for 28 days. Serum testosterone hormone, Follicle Stimulating Hormone (FSH), Luteinizing Hormone (LH), the levels of serum lipid peroxidation (MDA), reduced Glutathione (GSH), Glutathione Peroxidase (GSH-Px), superoxide dismutase (SOD) and Lactate Dehydrogenase (LDH) were estimated and samples from testis were separated for histological analysis. <b>Results:</b> The MSG treatment induced a significant decline in the values of serum testosterone, FSH, LH, GSH, GSH-Px and SOD. It also increased the values of serum MDA and LDH and spermatic arrest. While, the administration of Se-NPs orally before MSG treatment resulted in a decline in the values of serum MDA and LDH, an elevation in the values of serum GSH, GSH-PX and SOD, testosterone, FSH, LH and reappearance of sperm. <b>Conclusion:</b> The use of Se-NPs as a protector exhibited more improvement in values of estimated hormones and oxidative stress markers than using it as a therapy.

NR2B-DAPK1-P53 mediated hippocampal cell death following monosodium glutamate ingestion and interventions with luteolin, caffeic-acid and phoenix dactylifera

Introduction: Glutamate is the major excitatory neurotransmitter in the brain, but its accumulation potentiates excitotoxicity. In most food seasonings is the monosodium glutamate (MSG), whose over ingestion have been reported with glutamate-like neurotoxicity, thus, this study investigated the efficacy of Phoenix dactylifera and two of its phytochemicals MSG hippocampal toxicity. Materials and Methods: Forty-eight male Wistar rats were randomly allocated to eight groups of six rats each (n=6). The control received normal saline, group 2 received 4 g/kg MSG, groups 3 to 5 received 4 g/kg MSG followed by 100 mg/kg caffeic-acid, 100 mg/kg luteolin and 500 mg/kg Phoenix dactylifera, while groups 6 to 8 received the above agents first followed by 4 g/kg MSG orally for 21 days. 24 hours after the last ingestion, the rats were euthanized and hippocamapal tissue was removed and processed for GluN2B, DAPK1 and p53 immuno histochemical staining. Results: Repeated MSG ingestions caused high expressions of GluN2B, DAPK1 and p53 in the hippocampus of the exposed rats suggestive of an apoptotic cascades along the NR2B-DAPK1-P53 neuronal death pathway. Pre- or post- treatment with caffeic-acid, luteolin or Phoenix dactylifera markedly reduced the hippocampal expressions GluN2B, DAPK1 and p53. Conclusion: Phoenix dactylifera and its flavonoids are capable of downplaying the activities GluN2B, DAPK1 and p53 in MSG toxicity, thereby preventing hippocampal cell death.

Effect of Nigella sativa L. Seed on the Kidney of Monosodium Glutamate Challenged Rats.

Monosodium glutamate (MSG) consumption is responsible for a wide spectrum of health hazards including nephrotoxicity. The search for phytochemical strategies having broad safety profile to counter MSG toxicity is worthwhile. Nigella sativa L. seed (NSS) is very promising in this regard owing to its antioxidant and cytoprotective nature. Therefore, we attempted to investigate the potential protective effect of NSS on MSG-induced renal toxicity in rats. To accomplish this objective, fifteen adult Wistar albino rats were randomly and equally divided into three groups for 21 days: the control group received no treatment, MSG group supplemented with MSG at a dose of 30 g/kg feed, and MSG + NSS group supplemented with MSG at the same previous dose in conjugation with NSS at a dose of 30 g/kg feed. MSG and its combination with NSS failed to cause any significant difference in the kidney function parameters in comparison with the control. A significant elevation in lipid peroxides (LPO) level, glutathione-S-transferase activity and total antioxidant capacity (TAC) and a significant reduction in superoxide dismutase activity were found in MSG group. LPO level and TAC in MSG intoxicated rats significantly normalized by NSS ingestion. NO level showed absence of significant difference among all experimental groups. MSG elicited histopathological lesions such as decreased glycoprotein content and fibrosis however, NSS succeeded in enhancing all these features. MSG group showed positive glutathione reductase and superoxide dismutase 2 immuno-expression whereas, MSG + NSS group showed weak immunostaining. A significant increase in the number of apoptotic cells was observed in MSG group compared to the control. On the other hand, MSG + NSS group exhibited a significant decrease in the number of apoptotic cells. NSS mitigated MSG-induced renal impairments by ameliorating oxidative stress and exerting anti-apoptotic effect.

The Reproductive Toxicity of Monosodium Glutamate by Damaging GnRH Neurons Cannot Be Relieved Spontaneously Over Time.

ObjectiveThe present study aims to evaluate the effect of monosodium glutamate on testicular spermatogenesis in mice from the perspective of the hypothalamic-pituitary-testicular axis and whether this destructive effect is alleviated with time.MethodsNeonatal mice were randomly divided into a monosodium glutamate (MSG) group and a control group, just below the interscapular region after birth with 10 µL MSG to deliver 4 mg/g (body mass), or with equivalent volumes of 0.9% saline. Samples which involved blood, brains and testicles of mice were collected and measured at puberty at 60 days and adulthood at 90 days.ResultsThe results show that the fluorescence intensity of GnRH nerve fibers, the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) hormones in the reproductive system, the number of spermatocytes and spermatozoa in testicular sections, the body length, body weight, testicular weight, and testicular index in the 60-day-old mice in monosodium glutamate group (MSG60 group) and the MSG90 group were lower than those in the 60-day-old mice in normal control group (NC60 group) (p < 0.05), but the number of apoptotic cells in the testicular section was higher than in the NC60 group (p < 0.05). When the 90-day-old mice in monosodium glutamate group (MSG90 group) was compared with the MSG60 group, except for body weight and testicular weight increase (p < 0.05), there is no significant difference in the other parameters mentioned above (p > 0.05).ConclusionMonosodium glutamate can cause reproductive toxicity to male mice by damaging GnRH neurons, and this reproductive toxicity cannot be relieved spontaneously over time. These findings are supported by observed histological changes.

Toxicity of monosodium glutamate on liver and body weight with the protective effect of tannic acid in adult male rats

One of the food additives that are used extensively in the food industry is monosodium glutamate which has a flavor enhancer that is considered a double-edged sword on human health. Tannic acid (TA) is a natural antioxidant that works against many toxic substances. The current study aimed to evaluate the toxicity of MSG on rat liver with a possible protective role of TA. Forty adult male albino rats were used. They were divided into 4 equal groups, 10 rats each. Group I was the control group, Group II received TA (100 mg/kg) by oral gavage, Group III received MSG (2 g/kg) by oral gavage and Group IV received (TA and MSG) by oral gavage for 4weeks. At the end of the study, biochemical analysis was done and revealed that Group III showed a significant increase in the body weight and significant elevation in the serum levels of ALT and AST enzymes compared to group I with p > 0.001.While there was none -significant difference in relative liver weight with p> 0.05. Histopathological examination revealed that group III showed a severe complete loss in hepatic architecture such as congestion and dilatation in the blood vessels with different cellular changes such as necrosis and apoptosis as compared to group I. All these deleterious effects of MSG were greatly ameliorated by TA administration in group IV as compared to group III.

Ameliorative role of tannic acid on monosodium glutamate-induced pancreatic toxicity on albino rats

Monosodium Glutamate (MSG) is a widely used food additive which has several deleterious effects on different body organs. Tannic acid (TA) is naturally occurring antioxidants with several pharmacological properties. The present study was designed to study the toxic effects of MSG on the pancreas with the possible ameliorative role of TA. Forty male albino rats were used in this study in the form of four groups, 10 rats each. Group I, was the control group, fed on the standard diet, Group II received TA (100mg/kg), Group III received MSG (2g/kg) and Group IV received TA and MSG orally by gavage for 4weeks. Biochemical analysis revealed that MSG affected the pancreatic function by a significant increase in the serum levels of amylase and lipase enzymes, as well as, the blood sugar level (p 0.05). Histopathological examination showed severe destruction in the pancreatic architecture with hypertrophy and hyperplasia in the pancreatic islets as well as a decrease in the number of acinar cells in addition to congestion and dilation in the blood vessels. Co-administration of TA with MSG attenuated these effects; this role may be explained by its anti-oxidative effects that need future research to explain the mechanism of action. It is concluded that MSG has a deleterious effect on the pancreas functionally and morphologically and TA act as a good antioxidant agent against MSG toxicity.

Effect of L-Ascorbic Acid and Alpha-Tocopherol on The Monosodium Glutamate-induced Neurobehavioral Changes in Rats

Background: Monosodium Glutamate (MSG) is one of the most commonly used flavor-enhancing substances that may lead to neurological disorders. Objectives: The present work aimed to evaluate the role of L-ascorbic acid (AA) and -tocopherol (T) on the MSG-induced memory and neurobehavioral changes in rats. Methods: Thirty male Wistar albino rats were randomized into five equal groups: (1) control group, (2) MSG group received MSG (2mg/g BW) daily, (3) MSG+A group received MSG as in MSG group, and AA (100 mg/kg BW) daily, (4) MSG+T group received MSG as in MSG group, and T (600 mg/kg BW) twice weekly, and (5) MSG+AT group received MSG as in MSG group, AA as in MSG+A group, and T as in MSG+T group. After 3 weeks, neurobehavioral changes were assessed by open field test and Y maze. Oxidative stress markers were estimated, and immunohistochemistry was studied in hippocampal region. Results: MSG resulted in impairment of memory and induction of anxiety, with increased hippocampal malondialdehyde and decreased superoxide dismutase and glutathione peroxidase. Treatment with AA or T improved all the measured biochemical parameters, and the MSG-induced hippocampal degenerative changes, with decreased glial fibrillary acidic protein (GFAP) and synaptophysin expression. Combined administration of both vitamins was more effective in amelioration of MSG-induced impairments rather than taking AA or T alone. Conclusion: Both AA and T exhibit protective effects against neurobehavioral changes, oxidative stress and hippocampal degenerative changes induced by MSG toxicity, with more potent efficacy of their combination.

Ameliorative effects of cape gooseberry (Physalis peruviana L.) against monosodium glutamate (MSG)-induced toxicity: genetic and biochemical approach.

In this study, the toxic effects of monosodium glutamate (MSG), which is the sodium salt of glutamic acid and used as a flavor-enhancing additive in foods, and the protective role of cape gooseberry (Physalis peruviana L.) extract against these effects were investigated using Allium cepa L. test material with physiological, cytogenetic, and biochemical parameters. In the study, physiological changes were evaluated by determining root length, weight gain, and rooting percentage; genetic changes were evaluated by chromosomal abnormalities, micronucleus (MN) formation, mitotic index ratio (MI), and DNA damage. Oxidative stress was evaluated by determining the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT). Further, the relationships between oxidative stress and other parameters in the study were investigated. The antimutagenic effect of P. peruviana L. extract was evaluated as inhibition caused by MSG-induced chromosomal abnormalities (CAs) and DNA damage. In the study, six groups, including one control and five applications, were formed. The bulbs of Allium cepa L. in the control group were treated with tap water; the bulbs in the administration groups treated with 1000mg/L MSG, 125mg/L, and 250mg/L concentrations of P. peruviana L. extract and MSG (1000mg/L) in combination with P. peruviana L. extracts (125mg/L and 250mg/L) for 72h. At the end of the application, compared to the control group, MSG application caused decreases in rooting percentage, weight gain, root length and MI, increases in frequencies of MN formation, chromosomal abnormalities, and DNA damage. In the biochemical analysis, it was determined that there were increases in MDA, SOD, and CAT levels and a decrease in GSH level. P. peruviana L. extract ameliorated MSG toxicity by showing improvement in all these parameters depending on the application concentration. As a result, considering the toxic effects of MSG, it has been understood that the use as a food additive should be abandoned and the use of P. peruviana L. in addition to daily nutrition has been found to be a good antioxidant nutrient in reducing the effects of exposed toxic substances.

Impact of Monosodium Glutamate Intake on Heart Structure of Neonate Albino Rats and The Protective Role of Vitamin C

Background: Despite worldwide use of monosodium glutamate (MSG) as a flavor enhancer, its consumption has been an alarm due to daily exposure without definitive safety or exact limit. Vitamin C has an antioxidant activity. Objective: to clarify effects of neonatal MSG intake on heart structure of male albino rat pups and the possible modifying role of vitamin C and to assess reversibility of these effects.Material and Methods: 40 male albino rats at postnatal day 1(PD1) were allocated to three groups; control, group B administered MSG (4 mg/gm bw/day) and group C administered previous dose of MSG plus vitamin C (500 mg/kg bw/day) for 10 days. Groups B and C were subdivided according to animal sacrification age into B1, C1 sacrificed at PD10 (after the last dose of treatment) and B2, C2 sacrificed at PD30 (20 days after treatment cessation). At experimental end, left ventricular specimens were processed for histopathological, immunohistochemical and morphometric studies. The Results: Histologically, group B1 revealed massive degenerative changes including marked muscle fibers disruption, degeneration, separation with increased CT cells and fibroblasts, dilated congested capillaries and extravasated hemorrhage. Cardiomyocytes showed nuclear pyknosis, cytoplasmic coagulative necrosis and vacuolation. Previous changes were still present in group B2 but with less degree. MSG plus vitamin C resulted in greatly restored normal cardiomyocyte architecture in group C1 but complete recovery was observed in group C2. The mean area percentage of collagen fibers, vimentin and iNOS expressions showed high significant increase in B1, B2, low significant elevation in C1 but non-significantly different in C2 relative to control group. Conclusion: MSG induced myocardial toxicity in early postnatal period. Vitamin C greatly ameliorated histopathological and immunohistochemical alterations in cardiac tissue. MSG withdrawal for 20 days showed mild improvement but withdrawal after vitamin C administration was more effective in reversibility of MSG toxicity.

Zinc oxide nanoparticles with green tea extract complex in the pancreas of rats against monosodium glutamate toxicity.

Nanotechnology is an exciting field for investigators. Green zinc oxide nanoparticles (ZnO NPs) with Camellia sinensis extract complex are proved to be used in the treatment of the toxicity of monosodium glutamate (MSG) in the liver, kidney, and testis of rats. Therefore, the synthesized complex of green nanoparticles using green tea extract (GTE) was tested against the toxicity of MSG on the pancreas. The glucose and insulin levels were estimated aswell as some biochemical parameters for evaluating theantioxidant status of the pancreas tissue. The histopathological change of the pancreas also has been determined. It indicates the biomedical capability of ZnO NPs/GTE to act as potent antidiabetic through decreasing blood glucose and increasing serum insulin also, inhibition of lipid peroxidation and enhancement of the antioxidant parameters. The ZnO NPs/GTE enhanced the pancreatic cell and Langerhans islets as well lowered the sugar levels and stimulated insulin.

Natural products as safeguards against monosodium glutamate-induced toxicity.

Monosodium glutamate is a sodium salt of a nonessential amino acid, L-glutamic acid, which is widely used in food industry. Glutamate plays an important role in principal brain functions including formation and stabilization of synapses, memory, cognition, learning, as well as cellular metabolism. However, ingestion of foodstuffs rich in monosodium glutamate can result in the outbreak of several health disorders such as neurotoxicity, hepatotoxicity, obesity and diabetes. The usage of medicinal plants and their natural products as a therapy against MSG used in food industry has been suggested to be protective. Calendula officinalis, Curcuma longa, Green Tea, Ginkgo biloba and vitamins are some of the main natural products with protective effect against mentioned monosodium glutamate toxicity through different mechanisms. This review provides a summary on the toxicity of monosodium glutamate and the protective effects of natural products against monosodium glutamate -induced toxicity.

Modulation of monosodium glutamate induced histological injuries, histomorphometrical alterations and DNA damage in the mice hepatic and renal tissues by oral administration Nano-cerium oxide and L-arginine and their combination

Background: Monosodium glutamate is widely used as flavor enhancer/food additive. Many studies confirmed toxicity of monosodium glutamate even if in low concentrations especially in hepatic and renal organs. Therefore, our study aimed to examine ameliorative role of Nano-cerium oxide and L-arginine and their combination on the hepatic and renal toxicity induced by monosodium glutamate. Materials and Methods: Fifty mice were divided into five groups; 1st group served as control group; 2nd group treated oral with monosodium glutamate; animals of the 3rd group were administrated with monosodium glutamate and L-arginine. The 4th group was treated with monosodium glutamate and Nano-cerium oxide; and mice of the 5th group were treated with monosodium glutamate, L-arginine and Nano-cerium oxide. After 14 days, hepatic and renal tissues were removed for histological and histomorphometrical examinationsResults: Histological examination revealed hepatic and renal damages for animals treated with monosodium glutamate as well as highly significant declining of DNA content compared to control group. Administration of Nano-cerium oxide or L-argentine alone induced ameliorations of the hepatic and renal injuries induced by administration of monosodium glutamate but some pathological alterations still present. It also caused moderate improvement in the DNA content but still not reaches to normal value. Combined administration of Nano-cerium oxide and L-arginine caused marked ameliorations of the hepatic and renal changes induced by monosodium glutamate.Conclusions: The combined uses of L-arginine and Nano-cerium oxide more effective in preventing the hepatic and renal toxicity induced by monosodium glutamate in male albino rats than when they uses separately

Chronic toxicity of monosodium glutamate on the reproductive system and some internal organs of zebrafish (Danio rerio)

Chronic toxicity of monosodium glutamate on the reproductive system and some internal organs of zebrafish (Danio rerio)

Effect of Green Tea and Zinc oxide Nanoparticles Complex on Histopathology of Spleen of Male Rats Induced by Monosodium Glutamate

Background and objective: Synthesis of zinc oxide nanoparticles (ZnO NPs) with green tea extract (GTE) to form a complex is known to be one of the most multiuse nanoparticles with its application in treatment the toxicity of monosodium glutamate (MSG) on liver, kidney, testis, and pancreas. Therefore, the present study was concerned with the pontifical effect of ZnO NPs / GTE complex on the histological structure of spleen exposed to MSG. Materials and Methods: The toxicity of MSG was evaluated in male albino rats using two dosages (low, 6.0 and high, 17.5 mg/kg). The albino rats were taken for the experiment and randomly assigned into six groups; control, ZnO NPs, MSG-LD, MSG-HD, ZnO NPs / GTE + MSG-LD, and ZnO NPs / GTE + MSG-HD. The animals were decapitated after 30 days of exposure and spleens were dissected out and processed for the histological examination by light microscope. Results: The result revealed that MSG causes shrinkage in the white pulp nodule with increasing the area of the white pulp and degeneration of red pulp as compared to the control. The changes were more prominent in the rats treated with the higher dosage of MSG. The finding suggests that MSG may effect on adhesion of splenocytes and degeneration of red pulp in the rat leading to the reduced immunogenic response. Conclusions: The data could be demonstrated the effect of MSG on spleen tissue was a dose-dependent and led to hypertrophy of white pulp of the spleen. The ZnO NPs/GTE complex could provide a protective benefit against MSG-induced splenomegaly through its potent antioxidant properties due to the presence of GTE and reduction of the ZnO. The future study will be a concern on the thymus histology as it acts as the center of lymphoid organ. Keywords: Monosodium glutamate, ZnO nanoparticles, Spleen, Histology, Rats

The Interaction of Zinc Oxide/Green Tea Extract Complex Nanoparticles and its Effect on Monosodium Glutamate Toxicity in Liver of Rats.

Zinc oxide nanoparticles (ZnO NPs) are increasingly utilized in both industrial and medical applications. Therefore, the study was aimed to investigate the effect of green nanoparticle complex (green tea extract/zinc oxide nanoparticles complex, GTE/ZnO NPs) on oxidative stress induced by monosodium glutamate (MSG) on the liver of rats. Wistar male rats (n=64) weighing between 200-250 g were divided randomly into eight groups: control group was given physiological saline (1 mg/kg), two groups were treated with two different doses of MSG (MSG-LD, MSG-HD; 6 and 17.5 mg/Kg, respectively), GTE was given 1 mg/mL, 5th group was treated with ZnO NPs and 6th group was treated with GTE/ZnO NPs complex while, 7th and 8th groups were treated with MSG-LD + GTE/ZnO NPs complex and MSG-HD + GTE/ZnO NPs complex, respectively. All substances were given orally for 30 consecutive days. At the end of the study, the liver was homogenized for measurement of the oxidative stress status and anti-inflammatory biomarkers as well as histological and transmission alternations. Results showed that the antioxidant enzymes activity and glutathione level were significantly decreased in MSG groups than control in a dose-dependent manner. Conversely, the malondialdehyde and inflammatory cytokines levels were significantly increased in MSG groups than the control group. The liver indicated no evidence of alteration in oxidative status, anti-inflammatory and morphological parameters in GTE, ZnO NPs and GTE/ZnO NPs complex groups. In conclusion, MSG at both doses caused oxidative stress and inflammation on liver after 28 days of exposure that supported histological analysis and transmission view of hepatic parenchyma. GTE/ZnO NPs act as partial hepato-protective against MSG.