Archives of the Balkan Medical Union (Sep 2019)
Influence of combined nitrate and fluoride intoxication on connective tissue disorders in rats gastric mucosa
Abstract
Introduction. Certain regions in Europe and Ukraine have high concentration of fluorides in drinking waters. Highly developed agriculture can result in increased concentration of nitrates in ground and drinking waters. Therefore, their combined excessive intake with food and water is not excluded. The objective of the study was to determine the influence of combined nitrate-fluoride intoxication on concentration of different fractions of glycosaminoglycans (GAG) and L-hydroxyproline concentration in gastric mucosa of rats. Materials and methods. Chronic intoxications were induced by intragastric injection of sodium fluoride in a dose of 10 mg/kg, sodium nitrate in a dose of 500 mg/kg and their combination during 30 days. Concentration of GAG was determined by carbazole method. To evaluate concentrations of different fractions of GAG we used the method of differential precipitation with ethanol. For L-Hydroxyproline concentration estimation, we used Hydroxyproline Colorimetric Assay Kit (BioVision K555-100). Results. The total concentration of GAG decreases during chronic fluoride and nitrate intoxications, but increases during combined intoxication. Concentration of Heparin/Heparan GAG fraction and Keratan/Dermatan GAG fraction drops during nitrate and fluoride intoxications, but increases during combined intoxication. Chondroitin GAG fraction shows no statistically significant changes during fluoride intoxication, but increases during combined and nitrate intoxications. Concentration of L-hydroxyproline increases in all studied groups. Conclusions. We established that chronic excessive fluoride or nitrate intake can cause oxidative and nitrosative stress-depended collagen degradation, simultaneously decreasing the concentration of anti-inflammatory GAG. Combined intoxication leads to even more severe connective tissue degradation, but subsequently activates compensatory mechanisms through increase in concentration of anti-inflammatory GAG.
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