Monosodium glutamate (MG) is a popular food additive that is widely used for flavor enhancement. It is considered relatively safe for consumption in many countries since the time it was first discovered in 1907. However, various disorders have been attributed to MG exposure, while its toxic effects were reported in numerous studies. MG was associated with obesity, metabolic, gastrointestinal, reproductive and other disorders, while damage to satiety center was attributed to its use. However, some of the experimental studies conducted in the past had several flaws in their design or execution that presumably could have affected the results’ extrapolation onto the human population. Further studies are needed to establish monosodium glutamate role in induction and progression of vascular pathology, particularly its effects on the morphology of carotid sinus and adjacent structures, as information on this particular issue is scarce. The objective of this study was to analyze early morphologic changes of carotid sinus under the influence of a low dose of monosodium glutamate administered orally by means of electron microscopy in experimental setting. Carotid sinuses of 10 adult male albino rats were studied by electron microscopy following 4, 6 and 8 weeks of oral administration of 10 mg/kg monosodium glutamate daily. The data was compared with the results of morphologic study of carotid sinus in the control group of 10 adult male albino rats. The data obtained suggests that monosodium glutamate oral consumption is associated with alterations of carotid sinus wall consistent with dystrophy and hypoxia at the early stages of exposure and apoptosis, fibrosis and lipid transformation at the later stages, while carotid glomus shows signs of cellular damage and apoptosis at a slightly later point in time but then the alterations worsen progressively. Further investigation is needed to evaluate morphologic changes of carotid sinus and adjacent structures associated with monosodium glutamate withdrawal.

Carotid artery pathology is one of the leading causes of cerebral stroke. Among thepathogenetic factors in the development of carotid artery damage, disorders of lipidmetabolism, atherosclerosis, and metabolic syndrome occupy a prominent place. The alimentary factor is extremely important in this context. Monosodium glutamate is one of the most common food additives, which is often used uncontrollably and can cause changes in the structure and functions of organs and tissues. The purpose of the study: to analyze the dynamics of morphological changes in the carotid sinus area under the influence of monosodium glutamate when administered orally in an experiment. The area of the carotid sinus of 20 male laboratory white rats that received sodium glutamate orally at a dose of 10 mg/kg/day for 8 weeks was studied by morphological methods at the macro- and microstructural levels after 6 and 8 weeks of the experiment. The obtained data are compared with the results of a morphological study of the same area in 20 animals of the control group. Statistical processing of animal weight was performed using MS Excel 2007 software. Mean ± standard deviation was determined. After 6 weeks of the experiment, when evaluating the histological structure of the wall of the internal carotid artery in the area located directly above the bifurcation, when compared with the control group, multiplication and folding of the intima were found in the experimental group, presumably associated with the proliferation of endothelial cells under the influence of sodium glutamate, detachment of the endothelium and lysis of individual endotheliocytes, as well as uneven thickening of elastic media fibers and disruption of their structure. Attention was drawn to the accumulation of white fat perivasally and in the zone of the carotid glomus, as well as the disorganization of nerves and the expansion of vessels of the microcirculatory channel. After 8 weeks of the experiment, the negative dynamics of structural changes were noticeable: signs of increased inflammatory infiltration, deformation of the vessels of the microcirculatory bed with thickening of their walls and narrowing of the lumen, stasis, noticeable degranulation of cells of type I carotid glomus
cells, the appearance of single labrocytes (mast cells) in the infiltrate. The amount of adipose tissue (white fat) in the area of the carotid sinus and the perivasal bifurcation of the carotid arteries, as well as in the immediate vicinity of the carotid glomus, also increased markedly, and a tendency towards thickening of adipose tissue was noted. Thus, monosodium glutamate with systematic oral use can cause a violation of the structural organization of the carotid sinus, the wall of the carotid arteries and the carotid glomus, and the severity of changes in dynamics increases. Further research is needed to clarify the nature of the structural changes in the carotid sinus under the conditions of withdrawal of monosodium glutamate, as well as to find possible ways of correction

Sodium glutamate (latin – Monosodium glutamate) or monosodium salt of glutamic acid (E621) is one of the most common food additives used to enhance taste sensations and improve the organoleptic properties of food. First isolated in 1907 by Professor Kikunae Ikeda of the Imperial University of Tokyo, monosodium glutamate has been widely used in the food industry due to its ability to enhance the natural taste of food lost during processing and storage. The monosodium salt of glutamic acid, also known as the food additive E621, has been used in most modern food technologies to enhance taste and aroma. The first doubts about the safety of monosodium glutamate as a dietary supplement arose in 1968, after the publication in the British Medical Journal of data that the sodium salt of glutamic acid can cause many diseases [1, 2]. It was then that the term “Chinese restaurant syndrome” was first coined to describe the symptoms of eating glutamate sodium, including severe pain in the stomach, chest, head, flushing, fever, and increased sweating [2, 3]. To date, many studies have been conducted in many countries, but there is no consensus on a safe dose of monosodium glutamate [4, 5]. Studies have shown that excess glutamate can provoke hypertension and stroke, Alzheimer’s disease and nervous system abnormalities, erosive lesions of the gastric mucosa, and weight gain [6, 7, 8]. There are no data on the level of endogenous intoxication of the body with long-term use of monosodium glutamate in significant quantities [9]. However, scientists are particularly interested in the role of systematic use of monosodium glutamate in the  mechanisms of cardiovascular disease, which continue to predominate in the structure of death causes from year to year and, despite significant efforts of the health care system, annually lead loss of capacity for work and disability of a large patient’s number [10]. One of the leading causes of this situation continues to be a stroke, a frequent pathogenetic cause of which is the pathology of the carotid arteries [11, 12]. In current conditions, when many complex factors contribute to the development of atherosclerosis, diabetes, and obesity, scientists are focused on the pathogenesis of vascular lesions, including carotid arteries, their bifurcation zone, carotid sinus, and glomus, under the influence of risk factors. Of particular interest are morphological changes in the wall of the carotid arteries and structures of the carotid sinus in the context of damage and tissue regeneration under the influence of mechanical and chemical factors, to study which often use experimental models [13, 14, 15].

The aim of this experimental study was to evaluate micro- and ultrastructural changes of the carotid sinus wall during oral consumption of low doses of monosodium glutamate (MG) and following its withdrawal. Adult male albino rats (n=39) were enrolled into the study. Carotid sinus wall morphology was assessed by light and electron microscopy at the end of week 4 and week 8 of MG oral consumption, as well as 2 weeks after its withdrawal; the results were compared with the control group. After 8 weeks of MG consumption, the wall of the carotid sinus was disorganized, endothelial layer of intima deformed, often without clear margins, the media edematous and dissected with thickened elastic membranes, and the cells of the vascular wall were showing signs of apoptosis while extra fat was present in the adventitia. Upon discontinuation of MG after 4 weeks of its consumption, the structural organization of carotid sinus wall was partially preserved, whereas no compensatory processes were registered after 8 weeks of MG administration followed by 2 weeklong withdrawal. Therefore, 8-week-long lowdose MG consumption resulted in pronounced changes of the micro- and ultra-structure of the carotid sinus wall of albino rats. Discontinuation of MG following 4 weeks of its administration partially improved the morphologic characteristics of the carotid sinus wall within 2 weeks. Withdrawal of MG after 8 weeks of its administration did not result in any improvement of the micro- and ultra-structure of the carotid sinus wall within 2 weeks.