FREE RADICAL OXIDATION AT PARODONTITIS
Reactive compounds of nitrogen, oxygen and lipids in saliva, blood and gingival tissue of patients suffering from moderate form of parodontitis was studied by means of the electronic paramagnetic resonance (EPR) method and spintraps (DETS, DMPO, PBH – Sigma). In patients with parodontitis content of free NO in saliva and blood increases, while in gingival tissue – decreases. In saliva, blood and gingival tissue of patients intense EPR signals of superoxidracals (O2) and lipoperoxides (LOO)has been revealed indication intensification of processes of lipid peroxidation in oral cavity, as well as in whole organism of patient. Exaggerated synthesis of NO in saliva and blood of patient is determined by high- expression of inducible NO-synthase triggered by oxidative stress, and increased activity of neuronal NO-synthase in saliva as a result of high concentrations of metacholine and P- substance intensely secreted at parodontitis. Decreased content of free NO in gingival tissue of patients with parodontitis compared to control is the result of biological degradation of nitric oxide (conversion of NO into peroxinitrite on the background of intense oxidative stress in oral cavity) and nitrosylation of mitochondrial electron transport of gingival tissue (characteristic for parodontitis) with further decrease in content of free oxide, suppression of intensity of mitochondrial respiration, energogenesis, development of ischemia in oral tissue leading to further initiation of destructive processes and progression of parodontitis.
2. Сепиашвили P.H. Физиология иммунной системы, 2015, М. 327 ст..
3. Babu D., Soenen S.J. Raemdonek K., et al. TNF-a / cyclohexamide – induced oxidative stress and apoptosis in murine intestinal epithelial MODE-K cells. Curr Pharm Des. 2012 Iun 19.
4. Bullon P., Cordero M.D., Quiles., et al. Mitochondrial dysfunction promoted by Porphyromonas gingivalis lipopolysaccharide as a possible link between cardiovascular disease and periodontitis. Free Radic Biol. Med. 2011, May, 15; 50 (10); 1336-43
5. Droe ge W. Free radicalis in the physiological control of call function. Physio. Rev. 2002, 82, 47. 4, 477-503.
7. Redrini M., Massunda R., Fries G.R., et al. Similarities in serum oxidative stress markers and inflammatory cytokines in patients with overt schizophrenia at anrby and bate stages of chronicity. J. Psichiatr. Res. 2012 Jun. 46 (6), 819-24.
8. Rocha M., Herance R., Rovira S., et al. Mitochondrial dysfunction and antioxsidant therapy in sepsis. Infect. Dis- ord Drug Targes. 2012; Apr. 12 (2); 161-78.