Ўзбекистон республикаси олий ва ўрта махсус таълим вазирлиги заҳириддин Муҳаммад Бобур номидаги

 
Ключевые слова:
Активные формы кислорода, свободные радикалы, 
антиоксидант, ДНК, мутаген, иммунитет. 
In recent decades there has been increasing interest in the medical aspects 
of the effects of free radicals. These chemical substances are derivatives of different 

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oxidative biochemical reactions in the body cell. Free radicals usually take part in 
biochemical and physiological processes. They have high reactivity in human tissues, 
so, body uses complex enzymatic and non-enzymatic protective systems to prevent 
"overloading" free radicals and peroxides. In some pathophysiological conditions, the 
delicate balance between free radicals and antioxidant protection can be altered in 
favor of the former, leading to oxidative stress and tissue damage. [1] 
An unpaired electron in radicals is usually denoted by a full stop. For 
example, the hydroxyl radical is represented by HO, the hydrogen peroxide radical 
HOO, the superoxide radical OO – or as an example, the formulas of 3 ethyl alcohol 
radicals are given: CH
3
CH
2
O; CH
3
CHOH; CH
2
CH
2
OH. [2] 
It turned out that the so-called active oxygen forms, related to free radicals, 
have an unpaired electron and have a biological effect that can have both - regulatory 
and toxic effects. A certain amount of free radicals is always present in the cells of 
the body. They are necessary for the implementation of physiological processes: 
respiration, metabolism, protective immune reactions, etc. [3] 
Research works on the role of free radicals conducted actively in recent years, 
which lead to the discovery of the concept of oxidative stress as a pathological 
condition caused by excess free radicals emerged. As result, huge attention began to 
be paid to the role of free radicals in the development of human diseases and ways to 
protect against their action using antioxidants. In the mid-80s, a monograph, which 
outlined the knowledge accumulated by that time about the production and metabolic 
pathways of oxidants, antioxidant protection, cellular response, and clinical aspects of 
oxidative stress, was published. [6]. 
However, when there present plenty amount of free radicals (for example, 
when the antioxidant system does not work properly), the scale of "oxidation-
reduction" outweighs in the direction of oxidation. As a result, free radicals begin to 
interact not only with those molecules with which it is necessary for the normal 
functioning of the body, but also with various cell structures (DNA molecules, lipids 
and membrane proteins), thereby causing their damage. [3] 
As a result, antioxidant protection will be suppressed and free radicals will be 
“damaging substances” to cells and tissues. Thus, "oxidative stress" is a profound 
disruption of the prooxidant antioxidant balance in favor of the former, denaturation 
of proteins or enzymes, or mutagenic damage to nucleic acids. Activated neutrophils 
can be an example of both: physiological (lysis of microorganisms with intracellular 
and controlled production of reactive oxygen species) and pathological (inflammation 
with uncontrolled extracellular production of active oxygen forms) processes. 
Oxidative stress may be associated with endogenous stress or exogenous sources of 
free radicals. Exogenous sources that induce an increase in the formation of radicals 
are: 1) ionizing radiation; 2) excess amount of transition metals; 3) side effects of 

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drugs and toxic substances; 4) excess oxygen and an increase in oxygen 
concentration. Endogenous factors that lead to oxidative stress and accompany 
pathological conditions are follows: 1) constant renewal of the pool of 
immunocompetent cells (phagocytes) and activation at the site of injury; 2) blocking 
of biochemical processes as a result of violations of the mitochondrial electronic 
chain; 3) delocalization of the transfer of metal ions and blocking of biochemical 
processes in the gem; 4) a decrease in protective functions, including a decrease in 
the activity of antioxidant enzymes; 5) reducing the level of antioxidants; 6) blocking 
of biochemical processes as a result of mutation or "damage" of antioxidants. [4] 
The human body is exposed by different damaging internal and external 
factors, which leads to the cell's DNA damage (10,000-100,000 per day). These 
damages block the DNA replication and transcription, which leads to the appearance 
of mutations and the possibility of carcinogenesis development. The repair system 
detects damage in DNA and promotes its repair. Defects in DNA repair system more 
often observed during the development of cancer. Carcinogenesis is the genesis and 
development of a malignant tumor from a normal cell. The oxidation of DNA 
molecules can be one of the mechanisms of its development. [5] 
Active forms of oxygen generated by phagocytes during microbial 
invasion have a microbicidal effect, activate a transcription factor, which leads to the 
induction of a number of cytokines and immune receptors. Under the influence of 
active oxygen forms, protein synthesis activated, leading to the formation of 
apoptotic proteins, vascular endothelial growth factor, and vascular permeability 
factor. Active oxygen forms are involved in the synthesis of prostaglandins, 
prostacyclins, thromboxanes, leukotrienes. They promote the generation of 
chemoattractants, an increase in the proteolytic activity of proteins as a result of 
inactivation of natural protease inhibitors and a direct destructive effect on various 
tissue components. [8] 
Oxidative stress plays a key role in the formation of a large number of 
approimate damaged DNA sites, what is a critical factor in the carcinogenesis 
beginning. [5] 
Historically, it was believed that free radicals have only negative effects, but 
now there is a serious revision of views on their role in the life of the cell. There are 
several zones of action of active oxygen forms in the body. For example: 1)