Variaciones morfológicas de la glándula submandibular en ratas obesas por acción de glutamato monosódico / Morphological variations of the submandibular gland in obese rats by the action of monosodium glutamate

Este estudio tuvo como objetivo demostrar la existencia de variaciones morfológicas en el tejido conectivo de la glándula submandibular de ratas obesas expuestas a glutamato monosódico (GMS). Se utilizaron 12 ratas Sprague Dawley machos recién nacidas (6 ratas para el grupo 1, control; 6 ratas para el grupo 2 (GMS), 4 mg/g de glutamato monosódico de peso (5 dosis) mantenidas por 16 semanas respectivamente con una dieta y agua ad libitum. En el estudio se realizó un análisis estereológico e histológico, demostrándose una variación en el tejido conectivo presentando una disminución del volúmen glandular, mayor fibrosis, y disminución de adipocitos a nivel periférico siendo reemplazado por tejido rico en colágeno. Los vasos sanguíneos observados a nivel estereológico no presentan mayores cambios en cuanto a volumen, superficie y área.

SUMMARY: This study aims to demonstrate the existence of morphological variations in the connective tissue of the submandibular gland of obese rats exposed to MSG. Twelve male newborn Sprague Dawley rats were used (6 rats for group 1, control; 6 rats for group 2 (MSG), 4 mg/g of monosodium glutamate of weight (5 doses) maintained for 16 weeks respectively with a diet and water ad libitum. In the study, a stereological and histological analysis was carried out, demonstrating a variation in the connective tissue, presenting a decrease in the glandular volume, greater fibrosis, and a decrease in adipocytes at the peripheral level, being replaced by tissue rich in collagen. Blood cells observed at the stereological level do not present major changes in terms of volume, surface and area, but in the histological study greater vascularization is observed.

Vitamin E suppresses aortic ultrastructural alterations induced by toxic doses of monosodium glutamate / La vitamina E suprime las alteraciones ultraestructurales aórticas inducidas por dosis tóxicas de glutamato monosódico

SUMMARY: An association between certain food additives and chronic diseases is reported. Current study determined whether administering toxic doses of the food additive monosodium glutamate (MSG) into rats can induce aortopathy in association with the oxidative stress and inflammatory biomarkers upregulation and whether the effects of MSG overdose can be inhibited by vitamin E. MSG at a dose of (4 mg/kg; orally) that exceeds the average human daily consumption by 1000x was administered daily for 7 days to the rats in the model group. Whereas, rats treated with vitamin E were divided into two groups and given daily doses of MSG plus 100 mg/ kg vitamin E or MSG plus 300 mg/kg vitamin E. On the eighth day, all rats were culled. Using light and electron microscopy examinations, a profound aortic injury in the model group was observed demonstrated by damaged endothelial layer, degenerated smooth muscle cells (SMC) with vacuoles and condensed nuclei, vacuolated cytoplasm, disrupted plasma membrane, interrupted internal elastic lamina, clumped chromatin, and damaged actin and myosin filaments. Vitamin E significantly protected aorta tissue and cells as well as inhibited MSG-induced tissue malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). The highest used vitamin E dosage was more effective. Additionally, a significant correlation was observed between the aortic injury degree and tissue MDA, TNF-α, IL-6, and superoxide dismutase (SOD) levels (p=0.001). Vitamin E effectively protects against aortopathy induced by toxic doses of MSG in rats and inhibits oxidative stress and inflammation.

RESUMEN: Se reporta una asociación entre ciertos aditivos alimentarios y enfermedades crónicas. El objetivo de este estudio fue determinar si la administración de dosis tóxicas del aditivo alimentario glutamato monosódico (MSG) en ratas puede inducir aortopatía en asociación con el estrés oxidativo y la regulación positiva de los biomarcadores inflamatorios y si el efecto de una sobredosis de MSG se puede inhibir con vitamina E. Se administró MSG diariamente durante 7 días una dosis de (4 g/kg; por vía oral) que excede el consumo diario humano promedio, en 1000x a las ratas del grupo modelo. Mientras que las ratas tratadas con vitamina E se dividieron en dos grupos y se administraron dosis diarias de MSG más 100 mg/kg de vitamina E o MSG más 300 mg/kg de vitamina E. Todas las ratas fueron sacrificadas en el octavo día. Usando exámenes de microscopía óptica y electrónica, se observó una lesión aórtica profunda en el grupo modelo demostrada por una capa endotelial dañada, células musculares lisas degeneradas (SMC) con vacuolas y núcleos condensados, citoplasma vacuolado, membrana plasmática rota, lámina elástica interna interrumpida, cromatina agrupada y filamentos de actina y miosina dañados. La vitamina E protegió significativamente el tejido y las células de la aorta, además de inhibir el malondialdehído tisular (MDA) inducido por MSG, la interleucina-6 (IL-6) y el factor de necrosis tumoral alfa (TNF-α). La dosis más alta de vitamina E utilizada fue más efectiva. Además, se observó una correlación significativa entre el grado de lesión aórtica y los niveles tisulares de MDA, TNF-α, IL-6 y superóxido dismutasa (SOD) (p=0,001). La vitamina E efectivamente protege contra la aortopatía inducida por dosis tóxicas de MSG en ratas e inhibe el estrés oxidativo y la inflamación.

Dietary Supplementation with Monosodium Glutamate Suppresses Chemotherapy-Induced Downregulation of the T1R3 Taste Receptor Subunit in Head and Neck Cancer Patients.

(Background) We investigated the effect of dietary supplementation with monosodium glutamate (MSG) on chemotherapy-induced downregulation of the T1R3 taste receptor subunit expression in the tongue of patients with advanced head and neck cancer. (Methods) Patients undergoing two rounds of chemoradiotherapy were randomly allocated to a control or intervention group (dietary supplementation with MSG at 2.7 g/day during the second round of chemotherapy). The relative expression of T1R3, a subunit of both umami and sweet taste receptors, in the tongue was assessed by quantitative polymerase chain reaction analysis. Dysgeusia was assessed with a visual analog scale and daily energy intake was evaluated. (Results) T1R3 expression levels in the tongue, taste sensitivity, and daily energy intake were significantly reduced after the first round of chemotherapy compared with before treatment. Furthermore, these parameters significantly decreased after the second round of chemotherapy, but the extent of decrease was significantly attenuated in the MSG group compared with the control group. (Conclusions) MSG supplementation suppresses chemotherapy-induced dysgeusia, possibly due to the inhibition of the T1R3-containing taste receptor downregulation in the tongue, thereby increasing energy intake in patients with advanced head and neck cancer.

Monosodium glutamate causes hepato-cardiac derangement in male rats.

People in the fast-food era rely on pre-packaged foods and engage in limited physical activity, which leads to a shift in eating patterns. Monosodium glutamate (MSG), a dietary ingredient used in this sort of cuisine, has been found to be hazardous to both experimental animals and humans. The objective of this study was to explore at the unnecessary changes caused by consuming MSG in secret and exceeding the recommended dosage. Hence, we decided to evaluate the impact of MSG by using three different doses (200, 400, and 600 mg/kg body weight orally) for 28 days in rats. We uncovered that all three MSG dosages result in a rise in body weight, dyslipidemia, inflammatory response, and hepato-cardiac marker enzymes, all of which imply hepatic and cardiac toxicity. Furthermore, changes in redox status suggest oxidative stress, which was higher in all three MSG dosages although not as much as in the MSG-600 group when compared to control. Such effects eventually manifested themselves in tissue architecture of the liver and heart, resulting in severe hepato-cardiac derangement, but the degree of tissue damage was greater in the MSG-600 group. As a result, it is possible that MSG has a negative influence on the liver and heart. However, the MSG-600 group showed a substantial effect, indicating that MSG should not be used in food preparation. Therefore, the findings of the study may aid in the formulation of health-care strategies and serve as a warning to the general public regarding the use of MSG in daily diet.

Evaluación semicuantitativa de los microelementos del esmalte en un modelo de obesidad inducido por glutamato monosódico en ratas / Semi-quantitative evaluation of enamel microelements in an obesity model induced by monosodium glutamate in rats

RESUMEN: En la actualidad, existen múltiples modelos experimentales de obesidad, unos de ellos es la utilización de glutamato monosódico (GMS), un potenciador del sabor ampliamente utilizado en industria alimentaria. Este GMS ha sido relacionado con obesidad, diabetes, insulino resistencia, así como en alteraciones en múltiples órganos, tales como testículos, riñón e hígado, entre otros. Ha sido reportado el efecto del GMS en estructuras orales, tales como las glándulas salivales, alterando su morfología y función. La relación del efecto del GMS frente a tejidos dentarios no ha sido reportada, siendo esto relevantes debido a la información que proporciona a disciplinas tales como arqueología científica, identificación forense, paleoecología y odontología. El objetivo del estudio fue observar la modificación de los elementos en la superficie dental, en un modelo de obesidad inducida por GMS, en ratas. Se utilizaron 12 ratas neonatas Sprague Dawley machos, divididas en dos grupos según exposición a GMS (Grupo Control y Grupo GMS 1: 4 mg/g peso de GMS, 5 dosis, mantenidas 16 semanas. Fue calculado el índice de masa corporal (IMC) e Índice de Lee, además de ser analizados el porcentaje de masa de los elementos C, O, Na, P, Ca, Fe y K en la superficie dental, mediante análisis semicuantitativo. Los resultados indican que GMS indujo obesidad en las ratas, así como alteraciones en los porcentajes de masa de los elementos en la superficie dental, evidenciándose disminución de Ca, P y O, además de aumentos en C y Fe. Según reportes previos, la obesidad inducida por GMS, causa alteraciones en secreción y composición salival, elemento íntimamente relacionado con la composición del esmalte, lo que vendría a explicar nuestros resultados. Entender la composición superficial del esmalte superficial podría ayudarnos a comprender de mejor manera la relación entre caries dentaria y obesidad.

SUMMARY: Monosodium glutamate (MSG) is a flavor enhancer widely used in the food industry. It has been associated with obesity, diabetes, insulin resistance, as well as alterations in multiple organs, such as testicles, kidney, liver, among others. While its effect on oral structures such as the salivary glands has been reported, the impact on dental tissues has not been described. Since this information is also relevant in fields such as forensic identification, palaeoecology and dentistry, the objective of the study was to observe alterations on the tooth surface in a model of obesity in rats induced by MSG. Twelve neonate male Sprague Dawley rats were used, divided into two groups according to MSG exposure (Control Group and MSG1 Group: 4 mg / g weight of MSG, 5 doses were maintained for 16 weeks. Body mass index (BMI) and Lee's index as well as mass percentage of elements C, O, Na, P, Ca, Fe and K on the tooth surface were evaluated by semi-quantitative analysis. In addition to increases in C and Fe, results indicate that MSG induced obesity and alterations in the percentages of mass on the tooth surface in rats, showing a decrease in Ca, P and O, According to previous reports, MSG induced obesity causes alterations in secretion and salivary composition, an aspect closely related to enamel composition, thus explaining our results. Enhanced knowledge of enamel surface composition may help improve our understanding of the relationship between dental caries and obesity.

Antioxidant and cytoprotective effects of Nigella sativa L. seeds on the testis of monosodium glutamate challenged rats.

Monosodium glutamate (MSG) is one of the most widely spread food additives that might cause male infertility. However, Nigella sativa L. seeds (NSS) could provide a solution. This study was designed to investigate the potential effects of NSS on rats ingesting MSG. To achieve this aim, adult male albino rats were randomly equally assigned into three groups for 21 days: control group received no treatment, MSG group received MSG as 30 g/kg feed, and MSG + NSS group received MSG as 30 g/kg and NSS as 30 g/kg feed. Testis histomorphometry showed marked deterioration by MSG as atrophic seminiferous tubules with degeneration of their lining cells, damaged Leydig cells and decreased germ cells number. Periodic Acid Schiff stain indicated irregular interrupted basement membranes. Glutathione reductase, superoxide dismutase 2 (SOD2), and caspase-3 immuno-expressions increased in testicular cells. Testosterone levels were significantly decreased in MSG challenged rats along with significant increase in luteinizing hormone levels, whereas NSS normalized this hormonal profile. MSG exposure also caused significantly increased lipid peroxides (LPO), glutathione-S-transferase, and total antioxidant capacity (TAC) whereas nitric oxide and SOD2 were significantly decreased. NSS succeeded in rebalance LPO and TAC and ameliorated the histoarchitectural disturbances. NSS mitigated MSG-induced testicular impairment by its antioxidant and cytoprotective activities.

Modulation of immune functions, inflammatory response, and cytokine production following long-term oral exposure to three food additives; thiabendazole, monosodium glutamate, and brilliant blue in rats.

The food additives thiabendazole (TBZ), monosodium glutamate (MSG), and brilliant blue (BB) are commonly used in many daily-consumed food products worldwide. They are widely used in major agricultural and industrial applications. Yet, many of its toxicological aspects are still unclear, especially immune modulation. This research was therefore intended to investigate the effects of male Wistar rats' daily oral exposure for 90 days to TBZ (10 mg/kg b.wt), MSG (20 mg/kg b.wt), or BB (1.2 mg/kg b.wt) on the blood cells, immunity, and inflammatory indicators. The three tested food additives showed varying degrees of hematological alterations. Initially, megaloblastic anemia and thrombocytopenia were evident with the three tested food additives. At the same time, TBZ showed no significant changes in the leukogram element except eosinopenia. MSG induced leukopenia, lymphocytopenia, neutrophilia, and eosinophilia. BB evoked neutrophilia and lymphopenia. The immunoglobins M (IgM) and IgG were significantly reduced with the three tested food additives. In contrast, lysozyme and nitric oxide levels were elevated. A reduced considerably lymphocyte proliferation was detected with TBZ and MSG exposure without affecting the phagocytic activity. Various pathologic disturbances in splenic tissues have been detected. An obvious increase in CD4+ but a lessening in CD8+ immunolabeling was evident in TBZ and MSG groups. The cytokines, including interferon-gamma, tumor necrosis factor-alpha, and interleukin 1ß, 6, 10, and 13, were significantly upregulated in the spleen of rats exposed to TBZ, MSG, and BB. These results concluded that TBZ, MSG, and BB negatively affect hematological parameters, innate and humoral immune functions together with inflammatory responses. TBZ achieved the maximal negative impacts followed by MSG and finally with BB. Given the prevalence of these food additives, TBZ and MSG should be limited to a minimal volume use, or natural food additives should be used instead.

Effect of Monosodium Glutamate on Saltiness and Palatability Ratings of Low-Salt Solutions in Japanese Adults According to Their Early Salt Exposure or Salty Taste Preference.

Using umami can help reduce excessive salt intake, which contributes to cardiovascular disease. Differences in salt-exposed environment at birth and preference for the salty taste might affect the sense of taste. Focusing on these two differences, we investigated the effect of monosodium L-glutamate (MSG) on the saltiness and palatability of low-salt solutions. Japanese participants (64 men, 497 women, aged 19-86 years) tasted 0.3%, 0.6%, and 0.9% NaCl solutions with or without 0.3% MSG to evaluate saltiness and palatability. They were also asked about their birthplace, personal salty preference, and family salty preference. Adding MSG enhanced saltiness, especially in the 0.3% NaCl solution, while the effect was attenuated in the 0.6% and 0.9% NaCl solutions. Palatability was rated higher with MSG than without MSG for each NaCl solution, with a peak value for the 0.3% NaCl solution with MSG. There was no difference in the effect of umami ingredients on palatability between the average salt intake by the regional block at birth and salty preference (all p > 0.05). Thus, adding an appropriate amount of umami ingredients can facilitate salt reduction in diet while maintaining palatability regardless of the salt-exposed environment in early childhood or salty preference.

Memory state and hippocampal histomorphology in Wistar rat following monosodium glutamate-induced neurotoxicity; role of aqueous extract of Aloe Barbadensis

This study assessed the effect of varying doses of aqueous extract of Aloe barbadensis on the cellular changes of hippocampal cells, oxidative and memory state of Wistar rats following monosodium glutamate-induced neurotoxicity. Eighty Wistar rats (8 weeks) were randomly as-signed into 4 groups of 20 rats; Group 1 received 3 mL/kg of distilled water. Groups 2, 3 and 4 received 3 g/kg/day of MSG. In addition, groups 3 and 4 received 100 and 200 mg/kg/day of AB ex-tract respectively. Administration was done orally for 28 days in all groups. Five rats per group were sacrificed weekly over a 4-week period. Memory was assessed using radial arm maze on the last day of administration. Following brain harvest, one cerebral hemisphere was homogenized for oxidative state assessment, while the other was fixed in 10% neutral buffered formalin and stained with H&E for hippocampal histomorphology. Data obtained were analyzed using student t-test and p value < 0.05 was considered significant. Across the 4-week period, group 2 rats showed significant increase in time spent to identify baited arms, significant reduction in density of apparentlynormal neurons and oligodendrocyte in CA 1-3 regions of hippocampus, and significant increase in reduced glutathione when compared with other groups. However, no significant differences were noted between groups 1, 3 and 4 for the above stated parameters. The study concluded that MSG caused hippocampal neuronal and oligodendrocytes degeneration and impairment of memory. These anomalies are prevented by 100 and 200 mg/kg of Aloe barbadensis

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Monosodium glutamate alters the function and morphology of the parotid gland in Sprague Dawley rats / Glutamato monosódico altera la función y morfología de la glándula parótida en ratas Sprague Dawley

Monosodium glutamate (MSG) is a flavor enhancer widely used in the food industry, with obesogenic properties, in addition to causing alterations in the oral cavity. The aim of the study was to observe the morphofunctional changes in the parotid gland after the administration of MSG in rats. 18 newborn male Sprague Dawley rats were used, divided into three groups (Control group; MSG1 group: 4 mg/g weight of monosodium glutamate, 5 doses, kept for 8 weeks, and MSG2 group: 4 mg/g weight of MSG, 5 doses, kept for 16 weeks). The body mass index (BMI) was calculated, and the salivary flow, pH, a-amylase activity, Na, Cl, K and Ca were analyzed by quantitative analysis. After euthanasia by ketamine/xylazine overdose, parotid volume was analyzed and stereology was performed. MSG administration caused an increase in BMI and a decrease in parotid volume as well as a reduction in salivary flow and pH and an increase in a-amylase activity, also increasing the salivary sodium and chlorine levels. Alterations in the normal stereological parameters of the gland were observed. Exposure to MSG caused morphofunctional alterations at parotid gland.

El glutamato monosódico (MSG), es un potenciador del sabor ampliamente utilizado en la industria alimentaria. Diversos estudios han propuesto la relación entre éste y el desarrollo de obesidad, además de provocar alteraciones en la cavidad oral. El objetivo del estudio fue observar los cambios morfofuncionales a nivel de la glándula parótida, posterior a la administración de MSG en ratas. Se utilizaron 18 ratas neonatas Sprague Dawley machos, divididas en tres grupos según su tiempo de exposición y dosis a MSG (Grupo Control, Grupo MSG1: 4 mg/g peso de glutamato monosódico, 5 dosis, mantenidas 8 semanas, Grupo MSG2: 4 mg/g peso de MSG, 5 dosis, mantenidas 16 semanas. Fue calculado el índice de masa corporal (BMI), además de ser analizado el flujo salival, pH, actividad de α-amilasa, y Na, Cl, K y Ca mediante análisis semicuantitativo. Luego de la eutanasia por sobredosis de ketamina/xilasina, las glándulas parótidas fueron extraídas y analizado su volumen y fueron procesadas para histología, y estudio estereológico. La administración de MSG causó aumento en BMI y disminución del volumen parotídeo, además de disminución del flujo y pH salival, así como aumento en actividad de la a-amilasa, aumentando además los niveles de sodio y cloro salival. Fueron observadas alteraciones a nivel de los parámetros estereológicos normales de la glándula. La exposición a MSG causó alteraciones morfofuncionales a nivel parotídeo, observándose una disminución del volumen de la glándula, acompañado de alteraciones en el adenómero y conductos estriados de la glándula, implicados en la producción, secreción y modificación de la saliva, la cual se vio alterada, en el flujo, pH, y en sus componentes.

Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress.

This study evaluated the neuroprotective potential of Allium sativum against monosodium glutamate (MSG)-induced neurotoxicity with respect to its impact on short-term memory in rats. Forty male Wistar albino rats were assigned into four groups. The control group received distilled water. The second group was administered Allium sativum powder (200 mg/kg of body weight) orally for 7 successive days, then was left without treatment until the 30th day. The third group was injected intraperitoneally with MSG (4 g/kg of body weight) for 7 successive days, then left without treatment until the 30th day. The fourth group was injected with MSG in the same manner as the third group and was treated with Allium sativum powder in the same manner as the second group, simultaneously. Phytochemical analysis of Allium sativum powder identified the presence of diallyl disulphide, carvone, diallyl trisulfide, and allyl tetrasulfide. MSG-induced excitotoxicity and cognitive deficit were represented by decreased distance moved and taking a long time to start moving from the center in the open field, as well as lack of curiosity in investigating the novel object and novel arm. Moreover, MSG altered hippocampus structure and increased MDA concentration and protein expression of glial fibrillary acidic protein (GFAP), calretinin, and caspase-3, whereas it decreased superoxide dismutase (SOD) activity and protein expression of Ki-67 in brain tissue. However, Allium sativum powder prevented MSG-induced neurotoxicity and improved short-term memory through enhancing antioxidant activity and reducing lipid peroxidation. In addition, it decreased protein expression of GFAP, calretinin, and caspase-3 and increased protein expression of Ki-67 in brain tissues and retained brain tissue architecture. This study indicated that Allium sativum powder ameliorated MSG-induced neurotoxicity through preventing oxidative stress-induced gliosis and apoptosis of brain tissue in rats.

The effect of oral administration of monosodium glutamate on epileptogenesis in infant rats.

Glutamate is an excitatory neurotransmitter that is widely distributed throughout the brain. An increase in glutamate concentration or sensitivity of glutamate receptors triggers neurodegenerative diseases, epilepsy in particular. Monosodium glutamate is a substance added to foods to enhance flavour. We investigated the effect of monosodium glutamate on epileptogenesis, as well asheight and weight, in rats that were just weaned. Twenty-four male and female 21-day-old Wistar Albino rats were divided into two groups: one with monosodium glutamate added to the drinking water, and a control in which NaCl was added to the drinking water. The electrical stimulation threshold values were determined in animals to which the hippocampal kindling process was applied, and the stimulations at these threshold values were invariably applied to the animals until they were kindled. The electrical stimulation threshold values of the monosodium glutamate group did not statistically change, whereas the number of required stimulations for kindled rats was significantly lower compared with the control group. These results reveal that long-term oral administration of glutamate salts causes an increase in excitability in the central nervous system during ontogenetic development.

High concentration of MSG alters antioxidant defence system in lobster cockroach Nauphoeta cinerea (Blattodea: Blaberidae).

OBJECTIVE: Monosodium glutamate (MSG) is a food additive that has been shown to be toxic to rodents at high concentrations. The available studies in Drosophila melanogaster suggest that MSG toxicity depends on concentration and gender, thus the safety of MSG as a food enhancer still requires further investigation. We have documented impaired locomotor activity and altered oxidative stress markers in cockroaches co-exposed to methylmercury and monosodium glutamate (MSG). We herein examined the susceptibility of Nauphoeta cinerea to high and low concentrations (4% and 1%) of MSG, while monitoring the activities of acetylcholinesterase (AChE), as well as markers of oxidative stress and antioxidant activity over 30 days. RESULTS: There was no significant alteration in the parameters assessed at 1% MSG while 4% MSG caused an increase in the activity of reactive oxygen and nitrogen species, with a corresponding reduction in the activities of acetylcholinesterase, glutathione-S-transferase and catalase, suggesting the capacity of MSG to alter redox homeostasis in Nauphoeta cinerea.

Monosodium Glutamate (MSG) Renders Alkalinizing Properties and Its Urinary Metabolic Markers of MSG Consumption in Rats.

Monosodium glutamate (MSG) is widely used as a flavor enhancer and its effects on human health are still debated. We aimed to investigate whether MSG can act as alkalinizing agent in murine models and if its metabolites are biomarkers of MSG consumption. For this purpose, adult male Wistar rats were given water added with 1 g% MSG or three types of control water, including sodium chloride (NaCl) and sodium bicarbonate (NaHCO3). At 14 days, urinary pH, electrolytes, urinary metabolites and ion-exchanger gene expression were determined. The results revealed that MSG-treated rats had significantly more alkaline urine and higher levels of urinary sodium and bicarbonate similar to NaHCO3 controls. These changes correlated with a lower expression of ion-exchanger genes, namely, CAII, NBC1, and AE1, which are involved in bicarbonate kidney reabsorption. The urinary metabolic profiles also revealed similar patterns for the MSG and NaHCO3 groups. In conclusion, MSG exhibits similar properties to NaHCO3, an alkalinizing agent, with regard to inducing alkaline urine, reducing bicarbonate kidney reabsorption, and generating a specific urinary metabolic pattern. We believe that these observations will be useful to further study the MSG effects in humans.

Oral Monosodium Glutamate Administration Causes Early Onset of Alzheimer's Disease-Like Pathophysiology in APP/PS1 Mice.

Glutamate excitotoxicity has long been related to Alzheimer's disease (AD) pathophysiology, and it has been shown to affect the major AD-related hallmarks, amyloid-ß peptide (Aß) accumulation and tau phosphorylation (p-tau). We investigated whether oral administration of monosodium glutamate (MSG) has effects in a murine model of AD, the double transgenic mice APP/PS1. We found that AD pathogenic factors appear earlier in APP/PS1 when supplemented with MSG, while wildtype mice were essentially not affected. Aß and p-tau levels were increased in the hippocampus in young APP/PS1 animals upon MSG administration. This was correlated with increased Cdk5-p25 levels. Furthermore, in these mice, we observed a decrease in the AMPA receptor subunit GluA1 and they had impaired long-term potentiation. The Hebb-Williams Maze revealed that they had memory deficits. We show here for the first time that oral MSG supplementation can accelerate AD-like pathophysiology in a mouse model of AD.

CoQ10 ameliorates monosodium glutamate-induced alteration in detrusor activity and responsiveness in rats via anti-inflammatory, anti-oxidant and channel inhibiting mechanisms.

BACKGROUND: Competent detrusor muscles with coordinated contraction and relaxation are crucial for normal urinary bladder storage and emptying functions. Hence, detrusor instability, and subsequently bladder overactivity, may lead to undesirable outcomes including incontinence. Multiple mechanisms may underlie the pathogenesis of detrusor overactivity including inflammation and oxidative stress. Herein, we tested the possibility that CoQ10 may have a potential therapeutic role in detrusor overactivity. METHODS: Forty adult male Wistar albino rats weighing 100-150 g were used in the present study. Rats were divided (10/group) into control (receiving vehicles), monosodium glutamate (MSG)-treated (receiving 5 mg/kg MSG daily for 15 consecutive days), MSG + OO-treated (receiving concomitantly 5 mg/kg MSG and olive oil for 15 consecutive days), MSG + CoQ10-treated (receiving concomitantly 5 mg/kg MSG and 100 mg/kg CoQ10 daily for 15 consecutive days) groups. RESULTS: MSG resulted in significant increase in bladder weight and sensitised the bladder smooth muscles to acetylcholine. MSG has also resulted in significant increase in bladder TNF-α, IL-6, malondialdehyde, nerve growth factor and connexion 43, with significant decrease in the antioxidant enzymes superoxide dismutase and catalase. Olive oil had no effect on MSG induced alterations of different parameters. Treatment with CoQ10 has resulted in a significant restoration of all the altered parameters. CONCLUSION: Taken together, our results suggest that CoQ10 antagonizes the deleterious effects of MSG on detrusor activity. We propose that CoQ10 could be a therapeutic strategy targeting urinary bladder dysfunction.

Chronic toxicity of low dose monosodium glutamate in albino Wistar rats.

OBJECTIVE: The objective of this study was to observe the effects of chronic dosing with monosodium glutamate on mortality, fertility, major organ functions and histology in albino Wistar rats. RESULTS: 6 male and 6 female rats (age 6 weeks) were bred in a cage, feeding on standard growers' mash, with monosodium glutamate added (120 mg/kg/day). 12 corresponding breeding rats (on standard feed without MSG) were controls. Chronic dosing with monosodium glutamate in albino Wistar rats (at a dose consistent with the human ADI) led to increased mortality, fertility impairment, and significant changes in major organ function tests and histology. 23 deaths were recorded in the rats fed with MSG additive, while mortality was zero in the control animals. Fertility was lower in rats on MSG (48 births) than in controls (117 births). The weight gain of the MSG rats was higher than in controls. Biochemical parameters and organ histology remained normal in control animals. In MSG-treated rats however, liver/renal function tests, fasting serum cholesterol and triglyceride, serum uric acid showed a significant rise at trimestrial time-points. Histology showed mild portal inflammation in MSG rats, with periglomerular fibrosis and interstitial nephritis in two rats, at 6-12 months.

Coconut Water Prevents Renal and Hepatic Changes in Offspring of Monosodium Glutamate-Treated Wistar Rat Dams.

Monosodium glutamate (MSG) is a widely-consumed taste enhancer which has been implicated in the aetiology of renal and hepatic dysfunction in adults and their offspring. There is increasing evidence on the therapeutic properties of Coconut Water (CW) in kidney and liver disorders. This study investigated the effects of CW on renal and hepatic functions in offspring of MSG-fed dams. Twelve female Wistar rats (120 - 140 g) were grouped into four as follows; Control (10 ml/Kg distilled water), MSG (0.08 mg/Kg), CW (10 ml/Kg) and MSG+CW. Treatments were given orally daily commencing two weeks prior to mating, throughout mating and gestation until parturition. All dams received standard rodent diet and drinking water ad libitum throughout the study. After weaning on Post-Natal Day (PND) 28, serum was obtained from offspring for assay of liver and renal function. Histological analysis of the livers and kidneys were performed on both dams and offspring. There was no significant difference in liver enzymes, urea, creatinine and albumin levels amongst the offspring on PND 28. However, liver and kidney sections from MSG dams and their offspring showed early degenerative changes which were not evident in renal and hepatic tissues from CW and MSG+CW dams and offspring. These observations suggest that coconut water protects against monosodium glutamate-induced renal and hepatic dysfunction in dams and offspring.

Monosodium l-glutamate-obesity onset is associated with disruption of central control of the hypothalamic-pituitary-adrenal axis and autonomic nervous system.

The hypothalamic-pituitary-adrenal axis (HPA) exerts important catabolic peripheral effects and influences autonomic nervous system (ANS)-mediated processes. Impaired negative-feedback control or reduced HPA axis sensitivity and altered ANS activity appear to be associated with the development and maintenance of obesity. In the present study, we examined the hypothesis that the central HPA axis is dysregulated favouring ANS disbalance in monosodium l-glutamate (MSG)-induced rat obesity. Glucose homeostasis, corticosterone, leptin and ANS electrical activity were evaluated. Adult MSG-induced obese rats exhibited fasting hyperinsulinaemia, insulin resistance, glucose intolerance, hypercorticosteronaemia, hyperleptinaemia and altered ANS activity. A decrease in food intake was observed during corticotrophin-releasing hormone (CRH) treatment in both control and MSG-treated rats. By contrast, food intake was significantly elevated in control rats treated with dexamethasone (DEXA), whereas no alterations were observed following DEXA treatment in MSG-induced obese rats. After DEXA injection, an increase in fasting insulin and glucose levels, associated with insulin resistance, was seen in both groups. As expected, there was a decrease of parasympathetic activity and an increase of sympathetic nervous activity in CRH-treated control animals and the opposite effect was seen after DEXA treatment. By contrast, there was no effect on ANS activity in MSG-rats treated with CRH or DEXA. In conclusion, impairment of the HPA axis can lead to disbalance of ANS activity in MSG-treated rats, contributing to the establishment and maintenance of obesity.

Effect of monosodium L-glutamate (umami substance) on cognitive function in people with dementia.

BACKGROUND/OBJECTIVES: This study assessed the effect of continuous ingestion of monosodium L-glutamate (MSG) on cognitive function and dietary score in dementia patients. SUBJECTS/METHODS: This was a single-blind, placebo-controlled trial involving 159 subjects with dementia residing in a hospital or nursing home. We assigned the subjects to a group that ingested MSG thrice daily (0.9 g/dose) (MSG group; n = 79) or a group that ingested NaCl thrice daily (0.26 g/dose) (Control group; n = 80). This study consisted of a 12-week intake period, followed by a 4-week follow-up period without the ingestion of MSG or NaCl. We performed physical examination, cognitive symptom tests (the Touch Panel-type Dementia Assessment Scale (TDAS) and Gottfries-Bråne-Steen Scale (GBSS)), palatability and behaviour questionnaires, and blood tests before and after the intervention and after the follow-up period. RESULTS: There were no significant differences in the TDAS and GBSS total scores between the groups before and after the intervention. However, regarding the TDAS sub-items, "the accuracy of the order of a process" did not deteriorate in the MSG group compared with that observed in the Control group (p < 0.05). At the follow-up assessment, the TDAS total scores in the MSG group showed significant improvement compared with those reported in the Control group (p < 0.05). Furthermore, there was a correlation of changes from pre-intervention to post-intervention between the TDAS and enjoyment of the meal (r = -0.299, p = 0.049). CONCLUSIONS: Our results suggest that continued ingestion of MSG has an effect on cognitive function. Furthermore, the patients with improved questionnaires about palatability survey showed greater improvement in cognitive function.