Résumé
Introducción: El glutamato monosódico se emplea en humanos desde el pasado siglo como potenciador del sabor. Su inoculación parenteral en murinos durante el período neonatal causa lesiones en varios núcleos hipotalámicos. Objetivo: Describir los efectos del glutamato monosódico sobre el sistema neuroendocrinoinmune en murinos. Metodos: Se realizó una revisión de artículos de libre acceso en las bases de datos PubMed y SciELO entre enero de 2013 y julio de 2020. También se examinó el texto básico de la asignatura Sangre y Sistema Inmune de la carrera de medicina. Desarrollo: Con independencia de su efecto adictivo, varios estudios defienden la inocuidad del glutamato monosódico. Sin embargo, este compuesto puede atravesar la barrera hematoencefálica de neonatos de murinos, y ocasionar trastornos metabólicos, reproductivos y del sistema inmune. Conclusiones: El glutamato monosódico en roedores causa alteraciones en los órganos que integran el suprasistema neuroendocrinoinmune y, por tanto, afecta sus funciones homeostáticas. Los mecanismos patogénicos no se conocen con exactitud.
Introduction: Monosodium glutamate has been used in humans since the last century as a flavor enhancer. Its parenteral inoculation in murine during the neonatal period causes lesions in several hypothalamic nuclei. Objective: To describe the effects of monosodium glutamate on the neuroendocrine immune system in murine samples. Methods: A review of open access articles in the PubMed and SciELO databases was conducted between January 2013 and July 2020. The basic text of the Blood and Immune System course of the medical school was also reviewed. Development: Regardless of its addictive effect, several studies defend the safety of monosodium glutamate. However, this compound can cross the blood-brain barrier of murine neonates, causing metabolic, reproductive and immune system disorders. Conclusions: Monosodium glutamate in rodents causes alterations in the organs that make up the neuroendocrine-immune suprasystem and, therefore, affects their homeostatic functions. The pathogenic mechanisms are not known exactly.
Résumé
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.
Sujets)
Animaux , Mâle , Rats , Glutamate de sodium/administration et posologie , Glande submandibulaire/effets des médicaments et des substances chimiques , Obésité , Glutamate de sodium/pharmacologie , Vaisseaux sanguins/effets des médicaments et des substances chimiques , Poids , Fibrose , Rat Sprague-Dawley , Tissu conjonctif/effets des médicaments et des substances chimiques , Animaux nouveau-nésRésumé
@#Introduction: The toxicity of high concentration monosodium glutamate (MSG) has become a controversial issue because of its inconsistent results in human and animal studies. This present study aims to evaluate the effect of subchronic high-doses oral administration of MSG on spatial memory performance and hippocampal pyramidal cells number. Methods: This study involved twenty-eight male Wistar rats, which were divided into a control group of NaCl 0.9% and three intervention groups of MSG 1.0 mg/g bodyweight (M1), 2.0 mg/g bodyweight (M2), and 4.0 mg/g bodyweight (M3) for 30 days. Statistical analysis used a One-way ANOVA test. Results: The result showed significant differences in spatial memory on the Morris Water Maze (MWM) test, including path length (p = 0.020) and escape latency (p = 0.011) according to general linear model repeated measurement analysis. The mean difference of estimated hippocampal pyramidal cells total number among the groups showed volume (p = 0.001), numerical density (p = 0.590), and cells number (p = 0.004). Furthermore, Post-Hoc analysis in both spatial memory and hippocampal pyramidal cells showed that the increasing MSG dose from 1.0 to 4.0 mg/g bodyweight led to a decrease in the results of spatial memory performance on the MWM test and a decrease in hippocampal cells. Conclusion: The present study has provided novel quantitative data that subchronic administration of high-dose MSG caused deleterious effects on the spatial memory function and the volume and number of hippocampal pyramidal cells.
Résumé
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.
Sujets)
Animaux , Rats , Aorte/effets des médicaments et des substances chimiques , Maladies de l'aorte/induit chimiquement , Glutamate de sodium/toxicité , Vitamine E/pharmacologie , Aorte/anatomopathologie , Glutamate de sodium/administration et posologie , Vitamine E/administration et posologie , Microscopie électronique , Interleukine-6/antagonistes et inhibiteurs , Facteur de nécrose tumorale alpha/antagonistes et inhibiteurs , Rat Sprague-Dawley , Stress oxydatif/effets des médicaments et des substances chimiques , Modèles animaux de maladie humaine , Malonaldéhyde/antagonistes et inhibiteursRésumé
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.
Sujets)
Animaux , Mâle , Rats , Glutamate de sodium/effets indésirables , Émail dentaire/effets des médicaments et des substances chimiques , Aromatisants/effets indésirables , Obésité/induit chimiquement , Glutamate de sodium/administration et posologie , Indice de masse corporelle , Rat Sprague-Dawley , Caries dentaires/induit chimiquement , Modèles animaux de maladie humaine , Aromatisants/administration et posologieRésumé
Introducción: La obesidad, especialmente la visceral, constituye un factor de riesgo principal para múltiples enfermedades tales como: diabetes Mellitus tipo 2, enfermedades cardiovasculares, aterosclerosis, dislipidemias, enfermedad por hígado graso no alcohólico y cáncer. Se plantea que el estrés oxidativo podría ser el factor causal común de las comorbilidades asociadas a la obesidad. Objetivo: Evaluar el balance prooxidante/antioxidante en ratas con obesidad inducida con glutamato monosódico. Material y Métodos: Ratas Wistar hembras recibieron glutamato monosódico (4 mg/g de peso corporal) para inducir obesidad o NaCl 0,9 por ciento (Controles) subcutáneamente en período neonatal. A los 90 días, se confirmó la obesidad. Se les practicó eutanasia a los 180 días para la obtención de sangre e hígado para la determinación de marcadores bioquímicos. Resultados: Las ratas obesas presentaron niveles incrementados de TAG, AU, insulina e índices HOMA y TyG. Se constataron mayores concentraciones de nitratos y nitritos, productos avanzados de la oxidación de proteínas y productos de oxidación de la 2-desoxirribosa en el ADN en las ratas obesas. Conclusiones: Se concluye que la obesidad inducida con glutamato monosódico reproduce las principales alteraciones metabólicas asociadas a la obesidad visceral humana, dentro de las que se incluye el estrés oxidativo. Este modelo podría ser útil en la evaluación de estrategias terapéuticas para prevenir o disminuir complicaciones asociadas a la obesidad(AU)
Introduction: Obesity, especially visceral, is a major risk factor for several diseases such as Type 2 diabetes mellitus, cardiovascular diseases, atherosclerosis, dyslipidemia, non-alcoholic fatty liver disease, and cancer. Oxidative stress may be a unifying mechanism for the development of major obesity-related comorbidities. Objective: To evaluate the prooxidant-antioxidant balance in monosodium glutamate-induced obesity in Wistar rats (MSG- obese rats). Material and Methods: Female Wistar rats received subcutaneous (sc) injections of monosodium glutamate solution (4 mg/g of body weight) or vehicle (NaCl 0,9 percent; control) to induce obesity during the neonatal period. At 90 days of life, obesity was determined. At 180 days of life, rats were anesthetized and killed to obtain blood and liver samples for the determination of biochemical markers. Results: MSG obese rats presented significantly higher triglycerides, uric acid and insulin levels, as well as elevated HOMA and TyG indexes. Increased concentrations of nitrate and nitrite, 2-deoxyribose oxidation products and advanced oxidation protein products levels were observed in obese rats. Conclusions: Obesity induced by monosodium glutamate reproduces the main metabolic alterations associated with human visceral obesity, among which oxidative stress is included. This model may be useful for the evaluation of therapeutic strategies to prevent or decrease complications associated with obesity(AU)
Sujets)
Rats , Glutamate de sodium , Rat Wistar , Stéatose hépatique non alcoolique , Antioxydants , ComorbiditéRésumé
ABSTRACT Purpose To evaluate the influence of autonomic vagal and splenic activities on renal histomorphometric aspects in obese rats. Methods Thirty male Wistar rats were used, of which, 24 received subcutaneous injections of monosodium glutamate (MSG) during the first 5 days of life (4 g/kg body weight) and six control animals received injections of saline solution (CON). Five experimental groups were organized (n = 6/group): falsely-operated control (CON-FO); falsely-operated obese (MSG-FO); vagotomized obese (MSG-VAG); splenectomized obese (MSG-SPL); vagotomized and splenectomized obese (MSG-VAG-SPL). Results The MSG-FO group animals showed a significant reduction in body weight and nasal-anal length when compared to CON-FO group animals (p < 0.05). The MSG-VAG-SPL group showed significant reduced in most biometric parameters associated with obesity. Falsely-operated obese animals showed a significant reduction in renal weight, glomerular diameters, glomerular tuff and capsule areas and Bowman's space compared to CON-FO group animals (p < 0.05). There was a significant reduction in diameter, glomerular tuft and capsule areas, and Bowman's space in MSG-VAG, MSG-SPL, MSG-VAG-SPL groups when compared to the MSG-FO group. Conclusions Vagotomy associated with splenectomy induces a reduction in the adiposity and causes histological changes in the kidney of obese rats.
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Animaux , Mâle , Rats , Splénectomie , Vagotomie , Rat Wistar , Rein , Lipides , ObésitéRésumé
The interplay between obesity and gastrointestinal (GI) motility is contradictory, and the transgenerational influence on this parameter is unknown. We aimed to evaluate the GI function in a model of paternal obesity and two subsequent generations of their male offspring. Newborn male rats were treated with monosodium glutamate (MSG) and composed the F1 generation, while control rats (CONT) received saline. At 90 days, male F1 were mated with non-obese females to obtain male offspring (F2), which later mated with non-obese females for obtaining male offspring of F3 generation. Lee Index analysis was adopted to set up the obesity groups. Alternating current biosusceptometry (ACB) technique was employed to calculate GI transit parameters: mean gastric emptying time (MGET), mean cecum arrival time (MCAT), mean small intestinal transit time (MSITT), and gastric frequency and amplitude of contractions. Glucose, insulin, and leptin levels and duodenal morphometry were measured. F1 obese rats showed a decrease in the frequency and amplitude of gastric contractions, while obese rats from the F2 generation showed accelerated MGET and delayed MCAT and MSITT. Glucose and leptin levels were increased in F1 and F2 generations. Insulin levels decreased in F1, F2, and F3 generations. Duodenal morphometry was altered in all three generations. Obesity may have paternal transgenerational transmission, and it provoked disturbances in the gastrointestinal function of three generations.
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Animaux , Mâle , Femelle , Grossesse , Rats , Exposition paternelle , Obésité/étiologie , Transit gastrointestinal , Leptine , Motilité gastrointestinale , InsulineRésumé
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.
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Animaux , Mâle , Rats , Glande parotide/effets des médicaments et des substances chimiques , Glutamate de sodium/administration et posologie , Aromatisants/administration et posologie , Salive/composition chimique , Sodium/analyse , Glutamate de sodium/pharmacologie , Facteurs temps , Indice de masse corporelle , Chlore/analyse , Analyse de variance , Rat Wistar , alpha-Amylases/analyse , Aromatisants/pharmacologie , Concentration en ions d'hydrogèneRésumé
Background: Uterine leiomyomas (fibroids), a menace of the reproductive age, is characterized byproliferation of smooth muscle cells (hyperplasia) of the uterus. Alpha Stone Decoction is a poly-herbalformulation that is used for the shrinkage and prevention of uterine fibroids in folkore medicine.Objective: We investigated the efficacy and safety of Alpha Stone Decoction (ASD), on monosodiumglutamate (MSG) induced uterine hyperplasia.Materials and methods: Twenty-eight mature virgin female rats were randomly divided into four studygroups: A-control B- MSG (200 mg/kgbw), C- MSG þ ASD (100 mg/kgbw) and D- ASD 100 mg/kgbwalone. The administration was carried out by as a single daily dose via intraperitoneal route for 14 days.Total protein, triglycerides, estradiol (estrogen), progesterone, and total cholesterol levels in sera weredetermined using appropriate kits. Uterine hyperplasia was assessed via histomorphometric methodusing the mitotic image plus software to compute the fibroblast cell count density while the uteri andovaries of animals were stained with mason-tricon stain for histological examination.Results: Administration of MSG for 14 days resulted heavy deposits of collagen connective tissue withinthe myometrium layers of the uteri. ASD significantly (p < 0.05) reduced fibroblast cell count inMSG-treated animals and also protected against MSG-induced damage observed in the myometrium ofthe uteri and ovaries of the animals. Significant increases (p < 0.05) in levels of total protein;triglycerides, progesterone, cholesterol and estrogen in the MSG-treated animals were amelioratedfollowing administration of ASD.Conclusion: These findings suggest that ASD contains bioactive agents which reversed MSG-induceduterine hyperplasia. It may therefore be useful in reducing the proliferation of fibroblast cells andmanaging other symptoms associated with uterine myoma.
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SUMMARY: The objective of this study was to describe the effects of monosodium glutamate on the collagen of the parotid gland in an obesity model. 18 newborn male Sprague Dawley rats were used (first control group; second group of MSG1: 4 mg/g of monosodium glutamate weight, 5 doses, and third group of MSG2: 4 mg/g of monosodium glutamate, 5 doses, maintained for 8 and 16 weeks respectively). The content and type of collagen were analyzed, in addition to the levels of cholesterol, glucose, triglycerides and uric acid. Monosodium glutamate produced an increase in the obesity rates of the MSG2 group, in addition to an increase in blood cholesterol, glucose and uric acid levels compared to the control group. Type III collagen in the MSG2 group showed a statistically significant increase. Monosodium glutamate induced obesity, in addition to an increase in type III collagen fibers.
RESUMEN: El objetivo de este estudio fue describir los efectos del glutamato monosódico sobre el colágeno de la glándula parótida en un modelo de obesidad. Se utilizaron 18 ratas Sprague Dawley machos recién nacidas (primer grupo control; segundo grupo MSG1: 4 mg/g de peso de glutamato monosódico, 5 dosis, y tercer grupo MSG2: 4 mg/g de glutamato monosódico, 5 dosis, mantenidas durante 8 y 16 semanas respectivamente). Se analizó el contenido y el tipo de colágeno, además de los niveles de colesterol, glucosa, triglicéridos y ácido úrico. El glutamato monosódico produjo un aumento en las tasas de obesidad del grupo MSG2, además de un aumento en los niveles de colesterol en sangre, glucosa y ácido úrico en comparación con el grupo control. El colágeno tipo III en el grupo MSG2 mostró un aumento estadísticamente significativo. La obesidad inducida por glutamato monosódico, además de un aumento en las fibras de colágeno tipo III.
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Animaux , Mâle , Rats , Glande parotide , Glutamate de sodium/toxicité , Collagène/effets des médicaments et des substances chimiques , Obésité/induit chimiquement , Glandes salivaires/effets des médicaments et des substances chimiques , Triglycéride/sang , Acide urique/sang , Glycémie/analyse , Poids/effets des médicaments et des substances chimiques , Cholestérol/sang , Collagène/analyse , Rat Sprague-Dawley , Modèles animaux de maladie humaine , Animaux nouveau-nésRésumé
@#Introduction: Formation of enamel begins in intrauterine. The process is prone to disturbances, for example bad nutrition intake. Monosodium Glutamate (MSG) is a food additive that is added to meals to improve the taste. Unmeasured use can result in physical abnormalities, growth, and immune system disruption. This research aim of this study was to analyze MSG consumption on rats during gestation and gestation to lactation on enamel structure and mechanical properties in their first offspring. Methods: Three groups of male rats, aged 21 days, which were born from mice induced by MSG during gestation (group 1), during gestation to lactation (group 2) and those without MSG (group 3 as a negative control group). Monosodium Glutamate is given daily at the dose of 1.54 mg/gr (body weight/ BW) orally, which starts on the fifth day of gestation until partition (23 days) in the first group and until weaning time (44 days) in the second group. Analysis of the structure and properties of enamel was performed on the lower left first molar using scanning electron microscope (SEM) and Vikers microhardness test. Results: The average enamel hardness in MSG induced mice during gestation, gestation and lactation periods, and without MSG was 242.7 Vickers hardness (HV); 238.3 HV and 309.1 HV respectively, while the porosity in the enamel structure is 13,1909%, 18,147% and 7,039%. Conclusion: MSG intake in mice during gestation and gestation to lactation results in abnormalities in the structure of the enamel and its mechanical properties in offspring.
Résumé
Food additives and flavour enhancers used in the food industry are potential health risks. We tested the hypothesis that the food additive and flavour enhancer, monosodium glutamate (MSG), which is the sodium salt of glutamic acid can induce ultrastructural alterations to the kidney, and the antioxidant vitamin E can protect against acute kidney injuries induced by a toxic dose of MSG in a rat model of the disease. The model group of rats received a daily dose of MSG (4 gm/kg) for 7 days, whereas the protective groups were either received a 100 mg/kg vitamin E plus MSG or 300 mg/kg vitamin E plus MSG for 7 days. Rats were then sacrificed on day 8. Transmission and light microscopy images revealed substantial kidney damage induced by MSG in the model group as demonstrated by degenerated epithelial cells with Pyknotic nuclei, swollen mitochondria, damaged brush margins, dilated tubules, and widening of Bowman's space with shrinkage and deformity of some glomeruli. Treatment of the model group with vitamin E showed a substantial protection of kidney tissue and renal ultrastructure by 300 mg/kg vitamin E compared to a partial protection by 100 mg/kg vitamin E. In addition, MSG significantly (p<0.05) increased serum levels of urea and creatinine, which were significantly (p<0.05) decreased with vitamin E. However, for serum creatinine, high doses of vitamin E (300 mg/kg) were more effective than lower doses (100 mg/kg) of vitamin E. These results indicate that vitamin E at 300 mg/kg effectively protects against MSG-induced acute kidney injury in rats.
Los aditivos alimentarios y los potenciadores del sabor utilizados en la industria alimentaria son riesgos potenciales para la salud. Probamos la hipótesis de que el aditivo alimentario y el potenciador del sabor, glutamato monosódico (MSG), la sal sódica del ácido glutámico, puede inducir alteraciones ultraestructurales del riñón, y que las propiedades antioxidantes de la vitamina E, pueden proteger contra las lesiones renales inducidas por una dosis tóxica de MSG en un modelo de rata. El grupo modelo de ratas recibió una dosis diaria de MSG (4 g / kg) durante 7 días, mientras que los grupos protectores recibieron una dosis de 100 mg / kg de vitamina E más MSG o 300 mg / kg de vitamina E más MSG durante 7 días. Las ratas se sacrificaron el día 8. Las imágenes de microscopía óptica y de transmisión revelaron un daño renal sustancial inducido por el MSG en el grupo modelo, como lo demuestran las células epiteliales degeneradas con núcleos picnóticos, mitocondrias hinchadas, bordes dañados, túbulos dilatados y ensanchamiento del espacio de Bowman, además de la deformidad de algunos glomérulos. El tratamiento del grupo modelo con vitamina E mostró una protección sustancial del tejido renal y la ultraestructura renal de 300 mg / kg de vitamina E en comparación con una protección parcial de 100 mg / kg de vitamina E. Además, el MSG aumentó significativamente (p <0,05) en el suero los niveles de urea y creatinina, disminuyeron significativamente (p <0,05) con la vitamina E. Sin embargo, para la creatinina sérica, las dosis altas de vitamina E (300 mg / kg) fueron más efectivas que las dosis más bajas (100 mg / kg) de vitamina E. Estos resultados indican que la vitamina E a 300 mg / kg protege eficazmente contra la lesión renal aguda inducida por MSG en ratas.
Sujets)
Animaux , Rats , Glutamate de sodium/toxicité , Vitamine E/usage thérapeutique , Atteinte rénale aigüe/traitement médicamenteux , Vitamine E/pharmacologie , Rat Sprague-Dawley , Microscopie électronique à transmission , Modèles animaux de maladie humaine , Atteinte rénale aigüe/induit chimiquement , Atteinte rénale aigüe/anatomopathologie , Rein/anatomopathologie , Rein/ultrastructureRésumé
Monosodium glutamate (MSG) is a flavor enhancer. Its toxicity in a malnourished state appears not to have been fully investigated. This study was carried out to determine the effects of MSG on malnourished rats. Rats were randomly assigned into four groups of five rats/group. Group 1 rats were fed with malnourished feed; Group 2 rats received malnourished feed with dosed 1.6 mg/g MSG per body weight; Group 3 rats were fed with normal feed and dosed 1.6 mg/g MSG per body weight and Group 4 rats served as the control group (normal healthy rats) and were fed with normal feed for 28 days. After 28 days, the rats were sacrificed with the liver harvested and blood samples collected. Results from the study showed that malnourished rats had significantly lower levels of oxidative stress biomarkers including, anti-oxidants compared with the control. The levels of malondialldehyde concentration and xanthine oxidase activity were high in malnourished fed rats. Aspartate aminotransferase and alanine transaminase levels of malnourished and normal rats administered MSG were significantly low compared to the normal healthy suggesting that labialization occurs in liver leading to leakage of these enzymes from the liver to the serum. Malnourished rats showed significant decrease in body weight losing 48 grams after 28 days compared to malnourished and normal rats fed with MSG which recorded significant increase in body weight after 28 days adding 26 g and 42 g respectively.
Résumé
Background: Monosodium glutamate (MSG) produces adverse and damaging effects in different organs like liver and kidneys. Moringa has ameliorating effect on kidney and liver injury induced by monosodium glutamate. Objective: To study the ameliorating effect of moringa against rats liver and kidney injury induced by monosodium glutamate. Design: Prospective study. Setting: College of Pharmacy, Qassim University. Materials and Methods: This study was performed on 20 male rats and equally divided into 4 groups. The first group was control group, second group was moringa group, third group was MSG group and forth group was MSG plus moringa group. We determined liver function, albumin, total protein, kidney function, electrolytes and histopathological examination of tissue. Main Outcome Results: Moringa has ameliorating effect on kidney and liver injury induced by monosodium glutamate. Sample Size: A total of 20 malerats. Results: There was a significant increase in the levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), alkaline phosphatase (ALP), urea and creatinine. Significant decrease in the levels of albumin, total proteins and sodium levels in rats treated with monosodium glutamate. Kidney sections revealed normal structure of glomeruli and renal tubules as control group, liver revealed good improvements and mild cellular infiltrations were observed in rats treated with MSG and moringa group. Conclusion: Moringa causes ameliorating effect on kidney and liver injury induced by monosodium glutamate in rats. Limitation of the Study: Few studies about the protective effect of Moringa against toxic effect of MSG. So we need to focus on its beneficial effect against toxicity induced by MSG.
Résumé
@#Monosodium glutamate (MSG) is widely used as an additive in food. Excess consumption of MSG was reported to cause oxidative stress on brain, liver and renal resulted in increased production of reactive oxygen species (ROS). This study aims to determine the biochemical and histological effects of low dose MSG on the liver of adult male Sprague-Dawley rats. Animals (n=6 per group) were randomly divided into three groups with two treatment groups: 60mg/kg (MSG60) and 120mg/kg (MSG120), and one control group (distilled water). The substances were administered to the rats via force feeding for 28 consecutive days. On day 29, all rats were killed, and liver tissues were biopsied for the biochemical (total protein, liver enzymes, and the status of oxidative stress) and histological analysis. The total protein appeared significantly decreased (p<0.05) while alanine aminotransferase (ALT) and aspartate aminotransferase (AST) demonstrated a significant increased (p<0.05) in the MSG120 treatment group as compared to the control group. Malondialdehyde (MDA) levels and the antioxidant levels of superoxide dismutase (SOD) were significantly increase (p<0.05) in the MSG120 group as compared to the MSG60 and control groups. The histological findings revealed changes to normal liver architecture and accumulation of red blood cells in the central veins in both MSG groups. This study indicates that the MSG consumption at a dose of 120 mg/kg may alter the biochemical and histological parameters of the liver.
Résumé
Aims: The aim of this study is to evaluate the neuroprotective effects of Celastrus paniculatus seed oil (CPO) against monosodium glutamate in human IMR-32 cells. Study Design: Celastrus paniculatus seed oil used historically in Indian subcontinent for its neuro-enhancement property and also considered to have free radical scavenging activity. Methodology: In present study we have employed IMR-32, a neuroblastoma cells as our model system and utilized monosodium glutamate (MSG) a widely used food additive and proven inducer of free radicals to study the ameliorative effect of CPO against induced oxidative stress in neuronal cells. Results: Results showed that CPO ameliorates total protein level, decreases protein carbonyl and lipid peroxidation levels (p<0.001) as well as enhances the activity of superoxide dismutase and catalase (p<0.001) under oxidative stress conditions. Further we found that CPO increases the free radical scavenging capacity of cell by enhancing (p<0.001) glutathione level and help its regeneration by revitalizing the activity of glutathione peroxidase, glutathione S-transferase and glutathione reductase enzymes. Conclusion: It can be concluded that CPO has antioxidant property and proved to have ameliorative role against free radicals induced neuronal impairment.
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Monosodium glutamate (MSG) is widely used as a food additive but its excessive intake leads to oxidative stress of severalorgans. However, the oxidative effect of MSG on male accessory reproductive organs remains unclear. Therefore, theaim of this study was to evaluate the effect of MSG on the status of oxidative stress and morphological alterations in themale accessory reproductive organs such as epididymis, prostate glands and seminal vesicle of Sprague-Dawley rats.A total of 24 male Sprague-Dawley rats were randomly divided into three groups with 8 rats per group. Control groupreceived distilled water (1 ml/kg) while MSG60 and MSG120 received 60 mg/kg and 120 mg/kg of MSG, respectively.All the substances were administered via force feed oral for 28 consecutive days. At the end of the study, the rats weresacrificed to obtain the accessory organs for biochemical analysis and histological observations. The SOD activity in theepididymis showed a significant increase in MSG60 and MSG120 compared to control (p < 0.05). The GSH levels in theepididymis of MSG 120 showed a significant reduction (p < 0.05) compared to the control group. The levels of MDA andPC in the epididymis and prostate gland of MSG60 and MSG120 showed a significant increased (p < 0.05) comparedto the control group. Histological alterations were found in the epididymis and prostate gland of MSG treated rats. Inconclusion, MSG at both doses induced oxidative stress in the epididymis and prostate gland of experimental rats.
Résumé
ABSTRACT Sodium chloride is traditionally used as a food additive in food processing. However, because of its high sodium content, NaCl has been associated with chronic diseases. Margarine is a popular product that is used in several preparations, but it includes high sodium content; therefore, it is among the products whose sodium content should be reduced. Thus, the objective of this study was to produce margarines with reduced sodium content prepared using a salt mixture. The following 4 margarine formulations were prepared: Formulation A (control - 0% sodium reduction), Formulation B (20.8% less sodium), Formulation C (33.0% less sodium) and Formulation D (47.4% less sodium). The low sodium formulations were produced using a salt mixture consisting of NaCl, KCl, and monosodium glutamate at different concentrations. The margarines were evaluated using an acceptance test and descriptive tests: time-intensity and temporal dominance of sensations. The mixture used is a good alternative for preparing low sodium margarine because the low sodium formulations feature equal salinity and do not produce a strange or bad taste. Furthermore, it may be possible to prepare margarines with up to 47.4% less sodium and that are acceptable to consumers.
Sujets)
Sensation , Goût , Chlorure de sodium alimentaire/administration et posologie , Manipulation des aliments/méthodes , Margarine/analyse , Facteurs tempsRésumé
AIM To study lipid-lowering effects of gallic acid on glutamate-induced obesity mice.METHODS The obese model was established through subcutaneous injection of 3mg/(g · d)sodium glutamate into neonatal mice.After the model was established,the mice were divided into normal control group,model group,positive control group [simvastatin 30 mg/(kg · d)],high-,and low-dose group of gallic acid [400,200 mg/(kg · d)],and were intragastrically administered for ten weeks.Mice in each group after the last administration were fasted for 12 h except water.Blood was sampled from mouse eyes.The organs and adipose were obtained to determine the organ index and fat index.The levels of HDL-C,TG,LDL-C and TC in serum and liver were determined by using the corresponding reagent kit,and the serum leptin level was determined by ELISA kit and simultaneous determination of SOD,GSH-Px and MDA levels in liver.RESULTS Compared with the normal control group,the body weight and fat weight significantly increased in the model group;the levels of TC,TG and LDL-C in serum and liver significantly increased;the serum leptin level significantly reduced;the activity levels of SOD and GSH-Px in the liver significantly reduced;and the level of MDA significantly increased.Compared with the model control group,the body weight and fat weight significantly reduced in the gallic acid group mice and the levels of TC and TG significantly reduced in the serum and liver;SOD and GSH-Px levels significantly increased,MDA level significantly decreased in the liver.CONCLUSION Gallic acid can significantly reduce the blood lipid level of glutamate-induced obese mice.