Study of the Effect of Cadmium Chloride on Some Marker Liver Enzymes of Experimental Animals

Abstract

Introduction. Cadmium (Cd) is one of the most powerful and dangerous pollutants. Cd exposure is associated with multiple organ damage in both animals and humans. The mechanism of Cd toxicity is the disruption of the body’s antioxidant system (AOS), which leads to transformation of the functional integrity of the liver. The extent of target organ damage can be examined by measuring concentrations of key indicators of hepatocellular injury. The purpose of the work is to evaluate changes in the activity of enzyme markers of hepatotoxicity in the blood serum of laboratory animals after oral exposure to an aqueous solution of cadmium chloride (CdCl2) under the conditions of a subchronic experimental model with a period of remission. Materials and methods. The study was conducted on 40 white outbred rats. Animals of three experimental groups were intragastrically administered a pollutant in various dosages for 3 months. The duration of the remission stage was 1 month. The activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) was determined in the blood serum of animals. Results. When CdCl2 was administered to animals at a dose of 1 μg/kg, an increase in AST activity was observed by 45.9% relative to the control (p=0.006). An increase in the concentration of ALT and LDH is shown. A dose-dependent decrease in the level of alkaline phosphatase was revealed in three groups of animals by 24.7%, 37.5% and 55.4%, respectively (p=0.002). The noted trends indicate pathological processes occurring in hepatocytes. Conclusion. In the course of this study, it was found that under the conditions of a subchronic model of the experiment with a period of remission, cadmium, having a pronounced hepatoxic effect, induces liver damage in experimental animals.