Ruthenium‐based coordination complexes are compounds with great pharmacological potential. Once their toxicity and pharmacokinetics properties can be easily modulated changing the ligands on the six coordination sites of the metal, those species can present a broad spectrum of applications, such as: antineoplastic, bactericide, antiparasitic, vasorelaxant, among others. However, antioxidant properties of that kind of substance is still poorly explored, even after recent works have shown evidence that nitrosyl ruthenium complexes can scavenger free radicals. In addition, nitro‐imidazole derivatives are organic compounds with antioxidant properties and are able to work as ligands in coordination complexes. Considering that, the compounds cis‐[Ru(NO2)(bpy)2(4NIMN)](PF6) (1) and cis‐[RuCl(bpy)2(MTZ)](PF6) (2), where bpy=2,2′‐bipyridine, 4NIMN=4‐nitroimidazole and MTZ=metronidazole, were selected for analysis. Thus, the aim of the present study was to investigate in vitro antioxidant activity of those ruthenium complexes. The complexes were synthesized using microwave‐assisted synthesis, adapting methods previously described. Structural characterization was held through spectroscopic and spectrometric techniques, confirming the proposed structures. Cytotoxicity of the compounds at 3.12 to 100.0 μM was evaluated on A549 human lung carcinoma, RAW 264.7 murine macrophages, AGS human gastric carcinoma cells and human neutrophils at 5×106 cells/mL. No significant cytotoxicity was observed at any concentration of the compounds. Antioxidant properties were evaluated by quantifying malondialdehyde (MDA) and reactive oxygen species (ROS) production, and by evaluating superoxide dismutase activity in LPS‐stimulated RAW 264.7 cells treated with 1 and 2 at 3 – 25 μM. All the concentrations of both complexes were able to significantly reduce the production of superoxide anion in relation to the vehicle group, similarly to the reference treatment (α – tocopherol) All concentrations could also reduce the amount of MDA and ROS produced. Finally, the ruthenium complexes 1 and 2 were not cytotoxic to human neutrophils, lung and gastric carcinomas, and presented potent antioxidant properties. Tests are being carried out in order to elucidate antioxidant mechanisms and to analyze possible anti‐inflammatory effects.Support or Funding InformationCAPES; CNPqThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Insulin resistance is closely related to the metabolic syndrome that is characterized by a set of diseases that include obesity, dyslipidemia and diabetes mellitus. Due to a considerable increase of these diseases in the last decades, several studies are being carried out worldwide aiming to find solutions to prevent and to treat insulin resistance. Therefore, we decided to investigate the effects of the mixture of triterpenes alpha, beta‐Amyrin (AMI) on insulin resistance (IR) induced by sodium palmitate in skeletal muscle cells (C2C12), since previous studies regarding AMI conducted by our laboratory showed that AMI is able to improve insulin resistance in a hypercaloric diet obesity model. For this purpose, undifferentiated C2C12 cells (myoblasts) were maintained in horse serum (2%) for 6–10 days to induce differentiation to myotubes. The cytotoxic effect of AMI (3.12–400 μg/ml) on myoblasts and myotubes cells was assessed by the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide (MTT) assay. The effect of AMI (12.5, 25 and 50 μg/ml) was also evaluated in a glucose uptake model with 2‐[N‐(7‐Nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl) Amino]‐2‐Deoxy‐D‐glucose (2‐NBDG) in non‐resistant myotubes as well as in a model of insulin resistance induced by sodium palmitate (500 μM) complexed to 2% BSA for 24 h. After incubation, free 2‐NBDG was washed and fluorescence densities in cell monolayers were measured with a fluorescence microplate reader (Biotek Instruments, USA) set at an excitation wavelength of 485 nm and an emission wavelength of 535 nm. The protein (PT) concentration of each sample was determined by the Lowry method. Results were expressed as mean ± SEM of three independent experiments, each in triplicate. For multiple comparison of parametric data, One‐way ANOVA was used, followed by Tukey's post test. Values of p <0.05 were considered statistically significant. AMI (3.12–400 μg/mL) did not promote reduction of cell viability when compared to the control group, both in myoblasts and myotubes. In myotubes, AMI (25 ug/mL) increased glucose uptake (2.40 ± 0.60 2‐NBGD/PT) when compared to the control group (0.98 ± 0.06 2‐NBGD/PT). In the IR model, AMI (25 and 50μg/mL) also increased glucose uptake (1.3 ± 0.0 and 1.9 ± 0.1 2‐NBDG/PT) in myotubes, as well as rosiglitazone 20 μM (1.4 ± 0.0 2‐NBDG/PT) when compared to the IR control group (0.8 ± 0.1 2‐NBGD/PT). These preliminary results suggest that AMI improves glucose uptake in physiological and insulin resistance models in myotubes. These data corroborate with in vivo findings where AMI is able to improve insulin resistance in a hypercaloric diet obesity model. Studies are being conducted to elucidate the molecular mechanisms involved in these effects.Support or Funding InformationCAPES; CNPq; FUNCAPThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.