Myths and reality about the effects of glutamate. Compilation of scientific data of modern world literature

Abstract

The aim of our scientific work was to study the existing experimental models of glutamate effects on the body and to understand the mechanisms of this effect and its possible consequences. To achieve this goal, we have studied different sources of scientific medical literature. Results. In a healthy body, glutamic acid is secreted by brain neurons in the required amount as a neurotransmitter and participates in the main information flows of human body. Sodium glutamate, which enters the body with food in large quantities, affects the body, causing general toxic effects and has a local effect on the stomach, intestines, salivary glands and pancreas and so on. Based on the scientific literature, experimental models that study the effects of glutamate are divided into two types: models in which glutamate enters the body orally and when glutamate is administered subcutaneously and intraperitoneally in the neonatal period of life. In the first route of administration, glutamate causes a toxic effect, which is manifested in increased catalytic activity in the blood serum of alanine aminotransferase, aspartate aminotransferase and gamma-glutamyltranspeptidase in 2.5; 1.6; and 1.5 times, respectively, while the activity of alkaline phosphatase remained at control levels, indicating a pronounced hepatotoxic effect of monosodium glutamate as a dietary supplement. It causes an increase in content of total and tyrosine-containing peptides in the blood serum, increase of substances of low and medium molecular weight, as well as an increase in the values of intoxication, which indirectly indicates a violation of the detoxification of endogenous metabolites in the liver of experimental animals. Ingestion of sodium glutamate within the recommended doses has not been shown to cause marked pathological changes in the mucous, muscular and serous membranes of the gastric wall, but there is a slight fullness of the vessels of the submucosal membrane. It has been found that in high doses, sodium glutamate has a local pathogenic effect on the tissues of the stomach, which consists in thinning all layers of its wall, desquamation of the mucous membrane and its disorganization by reducing the size of gastric glands, increasing the number of vessels and their fullness with blood. One of the mechanisms of pathogenic effect of sodium glutamate is the contact local and free radical oxidizing effect on gastric tissues. In the oral route of administration of glutamate there are no phenomena of fat growth (obesity) as epidermal, which is characteristic of the abdominal form of obesity, so and pararectal, parallelic, pararenal and retroperitoneal, which is characteristic for the visceral form of obesity. In the subcutaneous and intraperitoneal routes of administration of glutamate in the neonatal period of life in experimental animals, glutamate causes hypersecretion of hydrochloric acid, the development of lesions manifested by hemorrhage, erosions and ulcers in the gastric mucosa and obesity. Prolonged administration of monosodium glutamate significantly enhances the striking effects of stress on the gastric mucosa. Morphological studies of the submandibular salivary glands of rats on the background of glutamate-induced obesity confirm the development of pathological changes, as evidenced by the detected vacuolar dystrophy in the acinar region, perivascular and periductal edema. On the background of abdominal obesity, dystrophic processes were found in the acinuses and minor dystrophic changes in the intraparticle inserts. Conclusion. In the subcutaneous and intraperitoneal routes of administration of glutamate in the neonatal period of life in experimental animals, glutamate causes hypersecretion of hydrochloric acid, the development of lesions manifested by hemorrhage, erosions and ulcers in the gastric mucosa and obesity. Prolonged administration of monosodium glutamate significantly enhances the striking effects of stress on the gastric mucosa. Morphological studies of the submandibular salivary glands of rats on the background of glutamate-induced obesity confirm the development of pathological changes, as evidenced by the detected vacuolar dystrophy in the acinar region, perivascular and periductal edema. On the background of abdominal obesity, dystrophic processes were found in the acinuses and minor dystrophic changes in the intraparticle inserts. There is no doubt in the fact, which is based on the results of numerous experimental studies and covered in professional scientific litefrature, that the abdominal form of glutamate-induced obesity is possible only with subcutaneous and intraperitoneal routes of its administration in the neonatal period of life and while intraorall way of administration does not occur.