Вміст метгемоглобіну та карбоксигемоглобіну в еритроцитах щурів за умов токсичного ураження на тлі аліментарної депривації протеїну

Abstract

The study of the content of total hemoglobin and its pathological derivates methemoglobin and carboxyhemoglobin in rats’ red blood cell under the toxic damage and alimentary protein deprivation are presented. In order to simulate the low-protein diet of animals for 28 days were kept, an isoenergy diet containing 4.7% protein, 10% fats and 85.3% carbohydrates, which was calculated according to the American Institute of Nutrition recommendations. The simulation of acute toxic damage was performed by per os acetaminophen-administration to experimental animals at doses of 1250 mg/kg of animal body weight. It was found that in experimental animals the 2-fold decrease in erythrocytes counts compared with the values of the control group was observed under the toxic damage after alimentary protein deprivation. In this case, both protein deficiency and the administration of acetaminophen toxic doses have a clear effect on the studied indicator. At the same time, a decrease of erythrocyte counts is accompanied by a simultaneous decrease of total hemoglobin content in rat erythrocyte hemolysate. In animals consuming a low protein diet, this may be due to a deficiency of essential amino acids involved in the synthesis of globin’s polypeptide chains. The maximal increase of methemoglobin content (5-fold compared with control) in rats’ erythrocyte hemolysate was recorded under the administration of acetaminophen toxic doses after alimentary protein deprivation. In these experimental conditions this may be associated with a decrease of methemoglobin reductase activity, which causes methemoglobin accumulates in erythrocytes in the form of Heinz bodies. An increase of the carboxyhemoglobin level in rats’ erythrocyte hemolysate of all the experimental groups compared with the control under the conditions of toxin administration after protein deficiency, probably indicates impaired synthesis and/or degradation of heme-containing proteins.