Gastric ulcer is one of the most common diseases of the digestive tract, which every year rejuvenates. This is a complex, multifactor disease, specific mechanisms of which are defined primarily in their etiology advantage of a factor of aggression or lack of protection of certain factors. Availability of Helycobacter pylori, hydrochloric acid, pepsin and bile acids are found to be the main factors of aggression and mucus secretion of bicarbonate, hydrophobic surface epithelium, blood flow and epithelial cell renewal - protection components gastric mucosa.
In addition, the pathogenesis of gastric ulcer disease is inextricably linked to free radical oxidation processes. Evaluation of free radical processes carried out by determining the antioxidant system, which prevents the formation of harmful and toxic effects of free radical oxidation metabolites.
The development of gastric lesions is associated with the dysfunction of the antioxidant system and with the change of the glutathione level which has been restored as a result of the accumulation of free radicals in the cell. There is an imbalance of antioxidant and prooxidant systems. Oxidative reactions lead to disturbance of the regulation of cell’s homeostasis which results in the appearance and progress of the disease. On the basis of these disorders are lipid peroxidation, oxidative modification of proteins and nucleic acids. In this condition the function of glutathione antioxidant system is very important. Glutathione system includes glutathione, glutathione peroxidase, glutathione reductase and glutation transferaze in which glutathione not only protects the cells against toxic free radicals, but in general determines the redox-status of intracellular environment. The reduced state of glutathione turns into oxidized states by the enzyme glutathione peroxidase. Reduced state of glutathione can be regenerated from oxidized states by the enzyme glutathione reductase which is continuously in a cell in the active state and is induced by oxidative stress. The ratio of recovered/oxidized glutathione within cells is a critical parameter that indicates the level of intracellular toxicity (oxidative stress level). That is why there are serious disturbances in non-availability or exhaustion of glutathione system. The literature data on individual indicators of glutathione antioxidant system in the body of gastric ulcers is rather ambiguous, and operation of the system in various organs in experimental ulcers remains unclear until the end.
The gastric lesions influences the function of glutathione system. Decreased glutathione content and glutathione reductase activity in gastric mucosa and erythrocytes was observed due to deficiency of the energy substrates that affect the protection systems of the organism. While the liver revealed growth of reduced glutathione and glutathione reductase activity. Compensatory gain functioning of glutathione system in the liver may be associated with high metabolic activity of the body or the fact that the liver contains many mitochondria, which produced large amounts of reactive oxygen species. Glutathione peroxidase activity increased in all homogenates of investigated tissue during the development of experimental gastric lesions. The data show that in the studied pathological process, except for the stomach, other organs and tissues were involved.
Keywords: experimental gastric lesions, reduced glutathione, glutathione peroxidase, glutathione reductase
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