Antioxidant system of the body

The body's antioxidant system is a set of mechanisms that inhibit auto-oxidation in the cell.

Non-enzymatic autooxidation, if not limited to a local outbreak, is a disruptive process. Since the period of the appearance of oxygen in the atmosphere, prokaryotes needed constant protection from spontaneous reactions of the oxidative decomposition of their organic components.

The antioxidant system includes antioxidants that inhibit autooxidation at the initial stage of lipid peroxidation (tocopherol, polyphenols) or reactive oxygen species (superoxide dismutase - SOD) in membranes. In this case, the particles formed with the nonsparse electron formed during the reduction, the tocopherol or polyphenol radicals are regenerated by ascorbic acid contained in the hydrophilic layer of the membrane. Oxidized forms of ascorbate, in turn, are reduced by glutathione (or ergotionein), which receives hydrogen atoms from NADP or NAD. Thus, radical inhibition is carried out by a chain of glutathione (ergotionein) ascorbate-tocopherol (polyphenol), transporting electrons (in the hydrogen atoms) from pyridine nucleotides (NAD and NADP) to CP. This guarantees a stationary extremely low level of free-radical states of lipids and biopolymers in the cell.

Along with the chain AO in the system of inhibition of free radicals in the living cell involved enzymes that catalyze the redox reactions of glutathione and ascorbate, glutathione-dependent reductase and dehydrogenase, as well as peroxide-catalase and peroxidase cleavage.

It should be noted that the functioning of the two defense mechanisms - the chain of bioantioxidants and the group of antiperoxide enzymes - depends on the hydrogen atoms pool (NADP and NADH). This fund is replenished in the processes of biological enzymatic oxidation-dehydrogenation of energy substrates. Thus, a sufficient level of enzymatic catabolism - an optimally active state of the body constitutes a necessary condition for the effectiveness of the antioxidant system. Unlike other physiological systems (for example, blood coagulation or hormonal) even a short-term deficiency of the antioxidant system does not pass without a trace - membranes and biopolymers are damaged.

Disruption of antioxidant protection is characterized by the development of free radical damage to various components of the cell and tissues that make up the CP. The polyvalence of manifestations of free radical pathology in different organs and tissues, the different sensitivity of cell structures to the effect of SR products indicate the unequal availability of organs and tissues with bioantioxidants, in other words, apparently their antioxidant system has significant differences. Below are the results of determining the content of the main components of the antioxidant system in different organs and tissues, which led to a conclusion about their specificity.

Thus, the peculiarity of erythrocytes is the large role of antiperoxide enzymes - catalase, glutathione peroxidase, SOD, hemolytic anemia is often observed in congenital enzimopathies of erythrocytes. Plasma contains ceruloplasmin, which has SOD-activity, absent in other tissues. The presented results allow us to present the AS of erythrocytes and plasma: it includes both the anti-radical link and the enzymatic defense mechanism. This structure of the antioxidant system allows to effectively inhibit SRO lipids and biopolymers due to the high level of saturation of red blood cells with oxygen. Essential role in limiting SRO is played by lipoproteins - the main carrier of tocopherol, from them tocopherol passes into erythrocytes on contact with membranes. At the same time, lipoproteins are most susceptible to auto-oxidation.

[1], [2], [3], [4], [5], [6]

Specificity of antioxidant systems of different organs and tissues

The initiating value of non-enzymatic autoxidation of lipids and biopolymers makes it possible to take the starting role in the genesis of the DP deficiency of the antioxidant defense system of the organism. The functional activity of the antioxidant system of different organs and tissues depends on a number of factors. These include:

1. level of enzymatic catabolism (dehydrogenation) - products of NAD-H + NADPH;
2. the degree of expenditure of the NAD-H and NADP-H in biosynthetic processes;
3. the level of reactions of enzymatic mitochondrial oxidation of NADH;
4. receipt of essential components of the antioxidant system - tocopherol, ascorbate, bioflavonoids, sulfur-containing amino acids, ergotionein, selenium, etc.

On the other hand, the activity of the antioxidant system depends on the severity of the effects of S60 inducing lipids, with their excessive activity, inhibition of inhibition and an increase in the production of CP and peroxides occur.

In certain organs of tissue specificity of metabolism, certain components of the antioxidant system prevail. In extracellular structures that do not have NAD-H and NADP-H, the influx of reconstituted forms of AO-glutathione, ascorbate, polyphenols, tocopherol is important. Indicators of the level of the provision of organism AO, the activity of antioxidant enzymes and the content of products of SRT integratively characterize the activity of the body's antioxidant system as a whole. However, these indicators do not reflect the state of the AU in individual organs and tissues, which can vary significantly. The foregoing allows us to assume that the localization and character of free radical pathology is predetermined mainly:

• genotypic features of the antioxidant system in various tissues and organs;
• the nature of the exogenous inductor SR, acting during ontogeny.

Analyzing the content of the main components of the antioxidant system in various tissues (epithelial, nervous, connective), it is possible to distinguish various variants of tissue (organ) systems of inhibition of CPO, on the whole coinciding with their metabolic activity.

Erythrocytes, glandular epithelium

In these tissues an active pentose phosphate cycle functions and anaerobic catabolism predominates, the main source of hydrogen for the antiradical chain of the antioxidant system and peroxidases is NADPH. Sensitive to inducers of SRO erythrocytes as oxygen carriers.

[7], [8], [9], [10], [11], [12], [13], [14], [15], [16]

Muscular and neural tissue

The pentose phosphate cycle in these tissues is inactive; as a source of hydrogen for antiradical inhibitors, and NADH formed in the aerobic and anaerobic cycles of fat and carbohydrate catabolism predominates for antioxidant enzymes. Saturation of cells with mitochondria causes an increased danger of "O2 leakage" and the possibility of damage to biopolymers.

Hepatocytes, leukocytes, fibroblasts

A balanced pentose phosphate cycle and ana- and aerobic catabolic pathways are observed.

Intercellular substance of connective tissue - blood plasma, fibers and the main substance of the vascular wall and bone tissue. Deceleration of CP in the intercellular substance is provided mainly by antiradical inhibitors (tocopherol, bioflavonoids, ascorbate), which causes high sensitivity of the vessel wall to their insufficiency. In the blood plasma besides them, there is ceruloplasmin, which has the ability to eliminate the superoxidanion radical. In the lens, in which photochemical reactions are possible, in addition to antiradical inhibitors, the activity of glutathione reductase, glutathione peroxidase and SOD is high.

The resulted organ and tissue peculiarities of local antioxidant systems explain the differences in early manifestations of joint ventures with different types of effects inducing SRO.

Unequal functional significance of bioantioxidants for different tissues predetermines differences in local manifestations of their insufficiency. Only the inadequacy of tocopherol, the universal lipid AO of all types of cellular and noncellular structures, is manifested by early damage in various organs. The initial manifestations of a joint venture caused by chemical prooxidants also depend on the nature of the agent. The data allow us to consider that along with the nature of the exogenous factor in the formation of free radical pathology, the role of the specific and specific tissue specific features of the antioxidant system conditioned by the genotype is essential. In tissues with a low rate of biological enzymatic oxidation, for example, the wall of the vessel, the role of the antiradical chain of ergotionein - ascorbate (bioflavonoids) - tocopherol is high, which is represented by bio-antioxidants not synthesized in the body; accordingly, chronic polyantioxidant insufficiency causes, first of all, damage to the vessel of wall veins. In other tissues, the role of enzyme components of the antioxidant system - SOD, peroxidase, etc., prevails. Thus, the decrease in the level of catalase in the body is characterized by the progressive pathology of periodontal disease.

The state of the antioxidant system in different organs and tissues is determined not only by the genotype, but also during the oncogenesis, phenotypically - the heterochronism of the fall in the activity of various components of the AS in them, conditioned by the nature of the inducer of the CI. Thus, in real conditions, individual combinations of exogenous and endogenous factors of disruption of the antioxidant system determine both the general free radical mechanisms of aging and the particular triggering links of free radical pathology that are manifested in certain organs.

The results of the assessment of the activity of the main links of the AS in various organs and tissues are the basis for the search for new drugs-inhibitors of the lipid-targeted SRO lipids for the prevention of the free radical pathology of a certain localization. In connection with the specificity of the antioxidant system of different tissues, AO preparations must perform the missing links differentially for a particular organ or tissue.

A different antioxidant system was detected in lymphocytes and erythrocytes. Gonzalez-Hernandez et al. (1994) studied AOS in lymphocytes and erythrocytes in 23 healthy subjects. It was shown that in lymphocytes and erythrocytes the activity of glutathione reductase is 160 and 4.1 units / h, glutathione peroxidase 346 and 21 units / h, glucose 6-phosphate dehydrogenase 146 and 2.6 sd / h, catalase 164 and 60 units / hour, and superoxide dismutase - 4 and 303 μg / s, respectively.