The main properties and biological effects of the antioxidant carnosine, the natural dipeptide β-alanyl-L-histidine, are considered. Data on the effective use of carnosine in different pathologies are presented. Special attention is paid to issues of use of carnosine in neurologic and mental diseases, in alcoholism as well as in physiological states accompanied by activation of free-radical processes and formation of oxidative stress.
Iron is a microelement with the most completely studied biological functions. Its wide dissemination in nature and involvement in key metabolic pathways determine the great importance of this metal for uni- and multicellular organisms. The biological role of iron is characterized by its indispensability in cell respiration and various biochemical processes providing normal functioning of cells and organs of the human body. Iron also plays an important role in the generation of free radicals, which under different conditions can be useful or damaging to biomolecules and cells. In the literature, there are many reviews devoted to iron metabolism and its regulation in pro- and eukaryotes. Significant progress has been achieved recently in understanding molecular bases of iron metabolism. The purpose of this review is to systematize available data on mechanisms of iron assimilation, distribution, and elimination from the human body, as well as on its biological importance and on the major iron-containing proteins. The review summarizes recent ideas about iron metabolism. Special attention is paid to mechanisms of iron absorption in the small intestine and to interrelationships of cellular and extracellular pools of this metal in the human body.
The effects of ethanol and acetaldehyde on the hemolytic stability of rabbit erythrocytes have been compared. Incubation of normal erythrocytes with ethanol facilitated both acidic and oxidative hemolysis and increased the percentages of cells that were hemolyzed at maximal rate. Acetaldehyde exerted a similar destabilizing effect on erythrocytes only in the case of oxidative hemolysis. The destabilizing effect of ethanol was observed in catalase-inactivated erythrocytes under acidic, but not oxidative, hemolysis conditions. It is concluded that the destabilizing effect of unmetabolized ethanol occurs under conditions of acidic hemolysis, whereas the destabilizing effect of the oxidation of ethanol to acetaldehyde takes place only under the conditions of oxidative hemolysis.
In vitro experiments were performed to determine if ethanol was metabolized by human erythrocytes and to investigate if ethanol or its metabolites, acetaldehyde and fatty acid ethyl esters, affected erythrocyte morphology and stability. No detectable metabolism of ethanol was found in erythrocytes, although ethanol itself caused an elevated rate of spontaneous haemolysis in erythrocyte preparations. Physiologically attainable levels of ethanol were found to stabilize erythrocytes against haemolysis induced by sodium hypochlorite, and the presence of ethanol caused a decrease in erythrocyte reactive oxygen species levels, although the mechanism for such a process is unknown. Both physiologically attainable and higher levels of acetaldehyde had no effects on erythrocyte morphology and stability even after a 16 h exposure. Fatty acid ethyl esters caused structural changes and instability in erythrocytes in vitro, but whether such changes occur in vivo has not been established. The results of these studies suggest that the deleterious effects of ethanol consumption on erythrocytes in vivo may be, at least in part, the result of direct effects of unmetabolized ethanol on erythrocyte components.
Analysis of the oxidative modification of plasma and erythrocyte ghost proteins of chronic alcoholic subjects and healthy non-alcoholics has been performed. It was found that increased levels of protein carbonyls in both plasma and erythrocyte ghosts from alcoholic subjects occurred in comparison to the levels found in preparations from non-alcoholics. Plasma proteins from alcoholic subjects did not show evidence of cross-linking, although plasma protein concentration and composition were changed. In alcoholic subjects who displayed no evidence of abnormal erythrocyte morphology no cross-linking of erythrocyte ghost proteins was detectable, whereas the ghosts obtained from alcoholic subjects who displayed morphologically abnormal erythrocytes contained cross-linked proteins. The in vitro treatment with acetaldehyde of erythrocytes from non-alcoholics caused increased levels of protein carbonyls and cross-linking products in erythrocyte ghost preparations which were similar to those found in severe alcoholics. It is concluded that chronic alcohol consumption can cause abnormal erythrocyte morphology and increased erythrocyte fragility as a result of oxidation and cross-linking of erythrocyte ghost proteins. These effects can be ascribed, in part, to exposure of erythrocytes to circulatory acetaldehyde which is a product of ethanol metabolism.
The effects of carnosine and related compounds on erythrocytes from alcoholics were studied. In their presence, erythrocytes showed an increased ability to resist haemolysis and showed a more normal morphology, with carnosine and N-acetyl-carnosine being the most effective compounds. These beneficial properties of the dipeptides do not appear to be directly related to their antioxidant or buffering properties.
Background: Alcoholism is an acute social problem worldwide for negative impact on health. This problem is closely associated with social stress and drinking traditions. Previously, it was established exhaustion of blood antioxidant in alcoholism patients. It requires development and investigation of substances with protective properties under ethanol impact, on both cells and biomolecules. Aims and Objectives: Lithium salts are widely used in medicine as mood stabilizers for mental pathologies, including alcoholism. In this work, we investigate lithium ascorbate for the protection of human blood plasma lipids and proteins under ethanol impact. Materials and Methods: Well-known antioxidants -carnosine and ascorbic acid -were used as reference drugs. Heparinized venous blood was used as an experimental substrate. The ethanol and tested substances in the form of water (physiological)solutions were added to blood in vitro. Protection effects were measured and estimated as concentrations of carbonyls proteins and products of lipid peroxidation in blood plasma. Results: It was shown similar protective action of lithium ascorbate and carnosine on human plasma biomolecules against damaging action of ethanol. No protective effect revealed for ascorbic acid. Conclusion: Lithium ascorbate and carnosine were proved to possess the protection effects for blood lipids and proteins under ethanol impact. Normothymic and bloodprotective properties are desirable for psychotropic drugs, and thus, lithium salts could be considered as prospective agents in the treatment of addictions and other pathologies associated with oxidative stress.
Organic lithium salts containing anionic components (succinate, fumarate, pyruvate and antioxidant ascorbate) were tested for protection of blood plasma proteins and lipids against ethanol-induced oxidation in vitro. We used normothymic lithium carbonate and well-known antioxidant dipeptide carnosine (b-alanyl-L-histidine) as the reference drugs. The oxidized proteins and lipids were determined by the level of carbonylated proteins (CP) and TBA-reactive products (TBA-RP), respectively. In alcoholic patients the level of oxidized proteins and lipids was higher than in healthy persons. Incubation of blood with ethanol resulted in an increase in oxidized proteins and lipids in blood plasma of healthy persons but had no influence on the level of CP and TBA-RP in blood plasma of alcoholic patients. Lithium carbonate, lithium ascorbate, and lithium succinate exhibited protective action against ethanol-induced oxidation of biomolecules of blood plasma of healthy people. These effects were comparable with carnosine action. The studied compounds had no effect on the level of CP and TBA-RP of blood plasma of alcoholic patients.
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