[Alteration mechanisms of oxidative stress at periodontal tissues of rats in a simulated periodontitis and elaborate methods of their correction].

INTRODUCTION: one of the peroxidation stress mechanisms is inducible NO synthase (iNOS) expression involved in the pathogenesis of periodontitis. AIM: to access the influence of isoform NO synthase (NOS) on alteration mechanisms of oxidative stress at periodontal tissues of 50 mature rats in a simulated periodontitis (SP). MATERIALS AND METHODS: a SP at rats was induced by a high-carbohydrate, high-fat (HCHF) diet. Тreated SP rat groups were intragastrically administered with selective neuronal NOS (nNOS) inhibitor 7-nitroindazole, selective inducible NOS (iNOS) inhibitor aminoguanidine, and nitric oxide synthase substrate L-arginine. Oxidative stress level in the homogenated soft periodontal tissues was evaluated by TBARS (thiobarbituric acid reactive substances) level before and after 1,5 hours of incubation. Antioxidant response was evaluated by the increase in concentration of TBARS for incubation, аnd by antioxidant enzyme activity - superoxide dismutase and catalase. RESULTS: nNOS activity increase in a SP considerably limits oxidative stress activation at periodontal tissues, decreases antioxidant response, but heightens catalase activity. iNOS functional activity stimulates oxidative stress at periodontal tissues of rats, decreases antioxidant response. L-arginine in a MS effectively repaired antioxidant response at periodontal tissues that probably will give positive result at complex treatment of periodontitis and MS generally. CONCLUSIONS: in the near future, the appropriate regulation of NO activity by using NOS-active agents may provide a novel strategy for the periodontal disease prevention and correction in a MS.