The Content of Residual Nitrogen in Rats’ Blood Plasma Under the Conditions Of Toxic Damage on the Background of Alimentary Protein Deprivation

Abstract

In the present study, the residual nitrogen content in the blood plasma of rats under the conditions of toxic damage on the background of alimentary protein deficiency is presented. The following biochemical indicators: total residual nitrogen; free amino nitrogen content; urea nitrogen concentration; ammonia nitrogen concentration was studied in the blood plasma of rats under the experimental conditions. During the experiment, the experimental animals consumed a semi-synthetic diet in accordance with the recommendations of the American Institute of Nutrition. In order to model the alimentary protein deprivation rats received a low-protein diet daily for 28 days, which contained 1/3 of the generally accepted daily requirement of protein. After four weeks of keeping animals on an experimental diet, acute toxic damage with acetaminophen was modelled. The toxin was administered at 1250 mg/kg of animal weight as a suspension in a 2% solution of starch gel once a day for 2 days using a special probe. The residual blood nitrogen content was determined in the protein-free filtrate after the precipitation of plasma proteins with Nessler's reagent. Determination of free amino nitrogen content in blood plasma was carried out by the Uzbek method according to the intensity of staining, which was formed due to the interaction of amino acids of blood plasma with ninhydrin. Determination of ammonia nitrogen content in blood plasma was evaluated by the interaction of ammonium ions with formaldehyde by the formation of hexamethylenetetraamine (urotropin). It was established that the increase in residual nitrogen content in the blood plasma of rats under the conditions of toxic damage on the background of alimentary protein deprivation is due to increased concentrations of its components - nitrogen of free amino acids and ammonia nitrogen. This indicates an increase in protein catabolism and disruption of ammonia neutralization mechanisms and the development of hyperammonemia. The defect of ornithine cycle enzymes and secondary liver damage by medicinal xenobiotics can be the causes of hyperammonemia. At the same time, under the conditions of acetaminophen-induced damage on the background of alimentary protein deficiency, a decrease in urea nitrogen content will be, which reflects a decrease in ureasynthesizing function of the liver.