Abstract
In chronic inflammations nitro-oxidative stress may induce secondary pathological processes. Therefore, in the present study we aimed to evaluate nitro-oxidative stress in animals with chronic experimental periodontitis. A rat model of ligature-induced experimental periodontitis was used. The study groups (n = 12) were: group I - negative control of healthy rats; group II – periodontitis (PER); group III - periodontitis + aminoguanidine (AG) (50 mg/kg/d i.p.); group IV – periodontitis + NG-nitro-L-arginine methyl ester (NAME) (5 mg/kg/d i.p.); group V – periodontitis + L-arginine (ARG) (100 mg/kg/d i.p.); group VI – periodontitis + Trolox (20 mg/kg/d i.p). Periodontitis was induced in 2 weeks and the treatments were administrated for one week. Blood samples were harvested at completion the study. Nitro-oxidative stress was assessed by total oxidative status (TOS), total antioxidative capacity (TAC), oxidative stress index (OSI) and total serum nitrates and nitrites (NOx). Systemic NOx, TOS and OSI increased significantly. AG, NAME and Trolox treatments reduced NOx, TOS and OSI. TAR was very low at PER animals, and increased significantly after AG, NAME and Trolox. ARG increased NOx, TOS and OSI, but did not influence TAR. In conclusion in rat experimental periodontitis systemic nitro-oxidative stress was important, and iNOS was the main enzyme involved in NO synthesis. NO synthesis was not involved in the antioxidant activity.
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