In vitro experiment has shown that Synthesit not only helps to protect red blood cells (cells that carry oxygen), but also contributes to deeper mechanisms of healing.

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The research has revealed that one of the key causes of aging, the development of oncological, age-related and metabolic diseases - the activity of Adenosine deaminase (ADA) and Xanthine oxidase (XO) enzymes, DECREASES UP TO TWO TIMES.

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This action of Synthesit prevents free radical oxidation and oxidative stress.

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‍This is a unique result that contributes to the protection of all human cells and many other factors that form such concepts as health and longevity.

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‍The experiment was carried out in vitro on blood cells.

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The experiment involved 21 people aged 40-80 years.

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The conclusions of the scientific experiment consist of 7 parts. From a scientific point of view each part reveals the unprecedented effect of Synthesit:

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1. In vitro experiment showed that Synthesit iron citrate promotes the reduction in the activity of key enzymes of the breakdown of purine nucleotides in blood plasma and in red blood cells. The effect was observed in most of the peripheral blood samples (90%);
2. More pronounced inhibitory effect of Synthesit iron citrate solution was observed in a group of middle-aged people (40-59 years). Since catabolic processes increase with aging, in this case, the breakdown of purine nucleotides (due to the stimulation of ADA and XO activities), which contributes to an increase in the level of FR in the body, followed by the further OS – one of the key causes of aging and age-associated diseases, including CVD, metabolic (obesity, type 2 diabetes mellitus) and oncological disorders. Therefore, the use of Synthesit iron citrate can be recommended as a geroprotector, especially for people who are at risk for age-related pathologies;
3. The decrease in the activity of ADA with Synthesit iron citrate contributes to an increase in the intracellular and extracellular levels of adenosine. It is known that cells with a high level of adenosine, under certain conditions, are more resistant to the oxidative action of FR, contributing to the stimulation of enzymes and low-molecular-weight antioxidants, such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) , glutathione reductase (GR) and glutathione, thereby protecting the cell from OS [41-44];
4. Aging, like most pathologies, is characterized by the presence of hypoxic states, which is accompanied by an increase in the activity of ADA [45]. Therefore, the suppression of the activity of this enzyme with Synthesit iron citrate stimulates the release of adenosine under hypoxic conditions, dilating blood vessels and promoting better flow, as well as contributing to an increase in the level of nitrogen monoxide (NO), a strong vasodilator, normalizing vascular tone, blood circulation, as well as oxygen transport to cells [46-49]. Many cells involved into the production of adenosine have adenosine receptors embedded in the plasma membrane. In the cardiovascular system, they are found on the surface of atrial cardiomyocytes, ventricles and the conducting system of the heart, in the endothelium and smooth muscle cells of the vessel walls. Thus, acting through stimulation of the release of adenosine and NO, Synthesit iron citrate can have antihypoxic and antiadrenergic properties, having a hypotensive effect, thereby acting as a kind of cardioprotector;
5. Adenosine is able to stimulate an increase in the level of ATP in cells [49; 50], and an increase in the activity of ADA leads to a decrease in the level of adenosine. A suppression of ADA activity using Synthesit iron citrate leads to the regulation of cell bioenergetics, performing control in the need and consumption of energy;
6. Also, the maintenance of vascular tone, microcirculation and normal oxygen delivery to cells can be carried out by suppressing the activity of XO with the use of Synthesit iron citrate. It was found that with aging, XO participates in the formation of vascular OS, which leads to a decrease in endothelium-dependent dilatation, by reducing NO [51]. FR generated by XO are involved in the oxidation of low-density lipoproteins and other proteins, contributing to the early risk of atherosclerosis, hypertension, heart failure, coronary heart disease, diabetes, as well as the formation of microthrombosis [52]. At the same time, FR generated by XO contribute to the disturbance of Ca₂+ - ATPase of the sarcoplasmic reticulum of smooth muscle cells, thereby inhibiting the transport of Ca₂+ that leads to vascular damage in various pathological situations;
7. In erythrocytes, FR generated by purine metabolism enzymes contribute to the oxidation of cysteine residues of hemoglobin with the formation of cross-disulfide bonds and aggregation of hemoglobin protomers with the formation of Heinz bodies. The presence of Heinz bodies affects the plasticity of the erythrocyte membrane, it loses its ability to deform when red blood cells pass through the capillaries. This causes a disturbance of the integrity of the membrane, which leads to hemolysis of red blood cells. Thus, inhibiting the enzymes of purine metabolism with Synthesit iron citrate, there is a decrease in the level of FR, as well as, possibly, extracellular accumulation of adenosine, which is one of the first steps in the protective auto- and paracrine cascade signal aimed at limiting cell damage in response to adverse conditions [53], contributing to the preservation of the integrity of blood cells and preventing the oxidation of hemoglobin in red blood cells and, as a result, increasing oxygen delivery to cells;
8. Moreover, O₂ — generated by XO acts as a precursor for other forms of FR, which have a more pronounced cytotoxic effect, disrupting the mechanisms of oxidation and phosphorylation during tissue respiration, the main function of which is to maintain thermoregulation, metabolic and energy balance in the cell [54]. A suppression of XO activity using Synthesit iron citrate stimulates tissue respiration and oxidative phosphorylation, thereby contributing to the normalization of biological oxidation processes and ATP synthesis.

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