Abstract
The purpose of the study was to determine metabolic parameters (alpha-amylase, alanine aminotransferase and aspartate aminotransferase, gamaglutamyl transpeptidase, glycoproteins and chondroitin sulfates) at the stages of sodium glutamate intake and after withdrawal. Materials and methods. Studies were conducted on 65 white male rats of reproductive age (2.5-3 months); the experimental group received 70 mg/kg of sodium glutamate per live weight for 8 weeks. The control group of animals received a standard diet. Before drug withdrawal, rats were studied every week, after drug withdrawal the studies were performed every two weeks (10, 12, 14, 16 weeks). Results and discussion. The study of the enzyme activity of alpha-amylase showed that this index increased on the average 1.3-fold compared with the control values, and at the end of the period when the rats were fed with sodium glutamate (8 weeks), the index increased by 3.85 times, alanine aminotransferase – by 12.3 times, aspartate aminotransferase – by 1.4 times, gamaglutamyl transpeptidase – by 2.7 times, glycoproteins – by 1.4 times, chondroitin sulfate – by 1.2 times. After transferring the animals to a normal diet, no recovery of the indices was found. According to the studied indicators sodium glutamate has a toxic effect on the liver, pancreas with elements of systemic inflammation. At the stages of discontinuation of monosodium glutamate recovery of most of the studied biochemical markers is not established. Alanine aminotransferase, determined on the 16th day after the abolition of monosodium glutamate, was reduced by 1.33 times compared to the last 8 weeks of admission, gamaglutamyl transpeptidase after 10 weeks was reduced by 1.5 times, after 12 weeks – by 0.4 times, after 14 and 16 weeks, the values corresponded to the control values at 10 week, the alpha-amylase level was reduced by 1.26 times, at 16 weeks – by 2.29 times, but they did not reach the control values. At the end of the study (16 weeks), the level of chondroitin sulfates was increased compared to 8 weeks of feeding animals with glutamate sodium by 1.27 times, and relative to control – by 1.56 times. There was a decrease in glycoprotein content at 16 weeks compared with 8 weeks of observation by 1.3 times, but did not reach the level of intact animals. Conclusion. Thus, the results of serum biochemical studies of rats treated with monosodium glutamate indicated the development of intoxication and its effect on biochemical markers, which were reflected in the dynamics of enzyme activity, inflammation and fibrosis. Most biochemical markers (except gamaglutamyl transpeptidase and aspartate aminotransferase) at the end of the experiment did not reach the level of intact animals, which is apparently due to the chronicity of the pathological process. In rats after discontinuation of monosodium glutamate from 10 to 16 weeks of the experiment, changes in biochemical parameters were observed, which indicated a toxic effect, which was accompanied by the development of subacute inflammatory process. After the transfer of animals to a normal diet, recovery is not established. Sodium glutamate according to the studied parameters has a toxic effect on the liver, pancreas with elements of systemic inflammation
Publisher
Petro Mohyla Black Sea National University