Synthesis, characterization and electrochemistry studies of iron(III) complex with curcumin ligand.

Iron overload is a serious clinical condition for humans and is a key target in drug development. The aim of this study was to investigate the coordination of iron(III) ions with curcumin ligand that may be used in the treatment of iron overload. Iron(III) complex of curcumin was synthesized and structurally characterized in its solid and solution state by FT-IR, UV-Vis, elemental analysis, and magnetic susceptibility. Electrochemical behaviour of the ligand and the complexes were examined using cyclic voltammetry. The cytotoxic activities of the ligand and the iron(III) complex were evaluated by the MTT assay. Curcumin reacted with iron in high concentrations at physiological pH at room temperature. Subsequently, a brown-red complex was formed. Data regarding magnetic susceptibility showed that the complexes with a 1:2 (metal/ligand) mole ratio had octahedral geometry. The complex showed higher anti-oxidant effect towards the cell line ECV304 at IC50 values of 4.83 compared to curcumin. The complex exhibited very high cytotoxic activity and showed a cytotoxic effect that was much better than that of the ligand. The potentials for redox were calculated as 0.180 V and 0.350 V, respectively. The electrochemistry studies showed that Fe3+ /Fe2+ couple redox process occurred at low potentials. This value was within the range of compounds that are expected to show superoxide dismutase activity. This finding indicates that the iron complex is capable of removing free radicals. The observed cytotoxicity could be pursued to obtain a potential drug. Further studies investigating the use of curcumin for this purpose are needed.

Molecular basis of vascular damage caused by cigarette smoke exposure and a new approach to the treatment: Alpha-linolenic acid.

Exposure to cigarette smoke (CS) causes vessel damage and mechanism of this damage has not yet been clearly identified. Therefore, in this study we aimed to investigate whether vessel damage due to the CS exposure will be prevented by the alpha-linolenic acid (ALA) or not which has anti-inflammatory effect in mice. For this reason, mice were grouped as controls (with and without CS) and ALA (with and without CS). The CS application continued 5 days a week for two months. At the end of two months, the mice were killed by cervical dislocation and their blood and thoracic aortas were isolated. ALA Treatment increased acetylcholine relaxations. CS decreased acetylcholine relaxation. CS with ALA treatment increased acetylcholine relaxations versus just CS treatment. CS caused rising in cyclooxigenase-2 and phospholipase A2 levels. This rise is inhibited with ALA treatment. CS decreased eNOS levels. But this result was not statistically significant. Furthermore, according to electron microscopic study CS damaged both smooth muscle and endothelium. While ALA treatment prevented smooth muscle damage it didn't prevent endothelial damage. Using cigarette and CS exposure is a risk factor for cardiovascular disease. Our study showed that this disease.