Blood expression of oxidative stress

Abstract

Introduction. Oxidative stress is a pathogenic mechanism of a number of diseases that affect tissues and organs. The usefulness of the blood markers in the diagnosis of the diseases and/or conditions associated with oxidative stress is substantiated by the blood expression of oxidative stress and the correlation with the intensity of the pathological process in the organs. An indirect marker for oxidative stress is malonic dialdehyde (DAM), the end product of lipid peroxidation triggered by oxidative stress. The assessment of the DAM level could reveal the intensity of the processes and can determine the therapeutic strategy. Aim of the study. To assess the level of DAM in the blood and the hepatic homogenate of laboratory animals in oxidative stress induced by muscle ischemia/reperfusion in crush syndrome.Materials and methods. The DAM level was measured by the classical thiobarbituric acid method, described by Vladimirov Iu. (1972), in the hepatic homogenate and erythrocytes of white laboratory rats subjected to muscle ischemia (240 min) and reperfusion (90 min) compared to control (240 min. ischemia) and healthy animals. Results. Prolonged ischemia (240 min) induced an insignificant (p> 0.05) increase in the level of DAM in both the hepatic homogenate (+7%) and in the erythrocyte hemolysate (+9%) in the experimental animals compared to the healthy ones. Removal of the causal factor and reperfusion (90 min) of the compressed muscle tissue did not change the DAM values in the hepatic homogenate, but produced a statistically significant decrease, up to values below those found in the control animals, in erythrocytes (-25%, p<0.01). Thus, long-lasting ischemia is associated with an insignificant increase in the end product of lipid peroxidation, which possible confirms the sufficient antioxidant capacity of the liver and erythrocytes, which in the case of blood cells is surpassed by the oxidative explosion conditioned by the reperfusion and the entry of oxygen. Conclusions. Statistically insignificant changes of DAM content in the liver and erythrocytes of animals with oxidative stress triggered by ischemia/reperfusion attest minor value of DAM as a marker of oxidative stress at late stages of the pathological process.