Obesity has become an epidemic since almost 1/6th of the Earth' s population is suffering from obesity and obesity-induced pathological states. One of the key events in the pathogenesis of obesity and its complica- tions (metabolic syndrome, type II diabetes) is NF-κB activation. Therefore, searching for drugs affecting NF-κB activation during metabolic syndrome (MetS) is a perspective way of its treatment. The purpose of this study was to evaluate the influence of NF-κB inactivation with ammonium pyrrolidinedithiocarbamate on nitric oxide production, activity of arginases, concentration of nitric oxide metabolites, and hydrogen sulfide content in the rat heart during MetS modelling. We conducted our study on 24 mature male Wistar rats weighing 200-260 g, divided into 4 groups: control group, MetS group, ammonium pyrrolidinedithio- carbamate (PDTC) administration group, and PDTC+MetS group. MetS was induced by introducing of 20% fructose solution as the only source of water for 60 days. PDTC was administered intraperitoneally thrice a week at a dose of 76 mg/kg. In a 10% rat heart homogenate, we analyzed: total NO-synthase (NOS) activity, inducible (iNOS) and constitutive NO-synthase (cNOS) activities, nitrite and nitrate reductase activities, nitrite, peroxynitrite, nitrosothiols and hydrogen sulfide content. In PDTC+MetS group, iNOS activity decreased by 22.6% compared to MetS group; arginase activity decreased by 20.9%; activity of nitrate and nitrite reductases decreased by 24.3% and 32.3%, respectively. Nitrite concentration increased by 25.8%, while ONOO- levels decreased by 56.7% and nitrosothiol levels increased by 57.9%. H2S concentration decreased by 11.6%. The activation of transcription factor NF-κB during the development of metabolic syndrome leads to hyperproduction of nitric oxide due to excessive activity of inducible NO- synthase and nitrite reductases.