Albumin is one of the most abundant proteins in the body of mammals: about 40% of its pool is located in the intravascular space and the remainder is found in the interstitial space. The content of this multifunctional protein in blood is about 60-65% of total plasma proteins. A decrease in its synthesis or changes of functional activity can destabilize oncotic blood pressure, cause a violation of transporting hormones, fatty acids, metals, and drugs. Albumin properties change under ischemic attacks associated with oxidative stress, production of reactive oxygen species, and acidosis. Under these conditions, ischemia-modified albumin (IMA) is generated that has a reduced metal-binding capacity, especially for transition metals, such as copper, nickel, and cobalt. The method of determining the cobalt-binding capability of HSA was initially proposed to evaluate IMA level and then licensed as an ACB test for routine clinical analysis for myocardial ischemia. Subsequent studies have shown the viability of the ACB test in diagnosing other diseases associated with the development of oxidative stress. This review examines recent data on IMA generation mechanisms, describes principles, advantages, and limitations of methods for evaluation of IMA levels, and provides detailed analysis of its use in diagnostic and monitoring therapeutic efficacy in different diseases.
Heart diseases, especially acute coronary syndrome (ACS), are among the most severe illnesses that often lead to death. Despite significant advances in the prevention and treatment of ACS, the incidence of the disease and its complications are very serious. The imbalance between pro- and antioxidant systems, the formation of active carbonyl compounds, and the end products of glycation in the blood and tissues are the key moments in the development of heart and neurological disorders leading to a change of behavioral responses. So, the search for antioxidants with cardio- and neuroprotective effects is an urgent task. This study was aimed at evaluating the effects of Corvitin and 2-oxoglutarate on physiological parameters, heart histology, and markers of carbonyl/oxidative stress of rats with pituitrin-isoproterenol-induced myocardial damage (PIMD). Increased sweating, tachycardia, significantly decreased locomotor and exploratory activity, changes of ECG, heart histology, and biochemical changes were observed in the PIMD-group. The administration of Corvitin or 2-OG led to the recovery of locomotor and cognitive activities of the rats, improvement in heart histology, a decrease in the levels of thiobarbituric acid reactive substances, advanced glycated end products, and various changes in the activity of the antioxidant enzymes, 6 days after PIMD. So, Corvitin and exogenous 2-OG show cardio- and neuroprotective effects through the decrease of carbonyl/oxidative stress and regulation of the activity of the antioxidant system.
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