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Cytoprotective processes induced by the effect of L-arginin-L-glutamate in rats with experimental pathology of the gastroduodenal zone

Regulatory mechanisms in biosystems, 2018-05, Vol.9 (2), p.300-307 [Peer Reviewed Journal]

ISSN: 2519-8521 ;EISSN: 2520-2588 ;DOI: 10.15421/021844

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  • Title:
    Cytoprotective processes induced by the effect of L-arginin-L-glutamate in rats with experimental pathology of the gastroduodenal zone
  • Author: Stepanov, Y. M. ; Ponomarenko, L. A. ; Lykholat, O. A. ; Shevchenko, T. M. ; Khomenko, O. M. ; Ponomarenko, A. A.
  • Is Part Of: Regulatory mechanisms in biosystems, 2018-05, Vol.9 (2), p.300-307
  • Description: The processes of effect of L-arginine-L-glutamate on peroxidation and slime-forming function of the stomach cells, the system of antioxidant defense in the blood, liver and brain tissues of rats with experimental pathology of the gastroduodenal zone have been investigated. The animals were divided into four groups. Group I – control group were rats injected intragastrically through a probe physiological solution. Group II included animals with erosive ulcerative lesions of the gastroduodenal zone. Modeling of the erosive ulcerative lesions was carried out by intragastric administration of medical bile (1 ml/100 g) in combination with immobilization-cold stress for 1 hour at + 4 ºС for a period of seven days. Rats of group ІІІ simultaneously received an intra-abdominal 4% solution of L-arginine-L-glutamate in a dose of 20 mg per 100 g of body weight at the same time as the erosive ulcerative lesions modeling. To clarify the role of NO-ergic mechanism of L-arginine-L-glutamate influence on the quantitative composition of mucins and free radical processes rats in group ІV with erosive ulcerative lesions were injected with non-selective NO-synthase inhibitor, L-NAME (L-NG-nitroarginine methyl ester), at a dose of 1 mg per 100 g at the same time as injections of 4% solution of L-arginine-L-glutamate. The simulation of erosive-ulcerative lesions of the gastroduodenal zone in the experimental animals was accompanied by the intensification of lipid peroxidation processes, the imbalance of the antioxidant defense systems and the development of oxidative stress in the blood, tissues of the stomach, liver and brain, which has tissue-specific features. In the blood of the animals, the activation of the enzymatic link of antioxidant defense did not compensate for free radical processes, as a result, the exhaustion of the reduced glutathione pool occurred, and the level of TBA-active products increased both in plasma and in erythrocytes. There was a depression of the enzymes of the antioxidant defense and a decrease in the level of recovered glutathione, indicating decompensating of the liver antioxidant protection systems in the liver tissue of the rats. In the experimental animals , formation of erosive ulcerative lesions was accompanied by destabilization of the oxidation-reducing processes in the brain, which led to the intensification of the lipoperoxidation. In the mucous membrane of the stomach of the experimental animals, the total number of protection factors – secretory mucins with a simultaneous structural change – decreased. The use of L-arginine-L-glutamate reduced the manifestations of oxidative stress in the stomach tissue of animals with experimental pathology and normalized the quantitative and qualitative composition of mucins. In the blood, liver tissues and brain of the rats, L-arginine-L-glutamate injections activated the enzymes of the first anti-radical linkage – superoxide dismutase and catalase contributed to the increase of the pool of reduced glutathione and the deceleration of free radical reactions. Investigation of reactions to the action of the inhibitor provides the basis for the hypothesis of the NO-mediated action of L-arginine-L-glutamate on the formation of S-nitrosothiols, as evidenced by the high level of reduced glutathione when the inhibitor is used.
  • Publisher: Oles Honchar Dnipro National University
  • Language: English
  • Identifier: ISSN: 2519-8521
    EISSN: 2520-2588
    DOI: 10.15421/021844
  • Source: DOAJ Directory of Open Access Journals
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