The objective of this study was to characterize MNA+ endothelial function in animal models. I used two animal models of endothelial dysfunction: a streptozotocin-induced diabetes model and a model of hypertriglyceridemia induced by high-fructose diet. I also used two models for in vitro study: a model of pyrogallolinduced endothelial impairment in isolated aorta of a rat and a model of endothelial impairment induced by hydrogen peroxide in the cell line EA. hy926. In the first model endothelial impairment was observed only as the endothelial impairment of NO-dependent vasodilation function, in the second model as a LDH release. Both in diabetes and in hypertriglycerydemia prolonged MNA+ administration (100 mg/kg per. os.) increased the level of endogenous MNA+ and its metabolites in plasma. It prevented also endothelial dysfunction development (the endothelium-dependent relaxation dysfunction of aorta induced by acetylcholine and histamine). In diabetes MNA+ therapy did not reverse the PGI2 production by aortic wall although it prevented compensatory increase of 6-keto-PGF1a concentration in plasma. In hypertriglycerydemia, on the other hand, MNA+ administration seemed to increase PGI2 production by vascular wall. MNA+ decreased the level of triglycerides concentration in hypertriglyceridemic model however, this effect was not observed in diabetes model. In diabetes model MNA+ ; had little effect on biochemical parameters of diabetes. The research showed that in vitro MNA+ had little effect on preventing endothelial impairment in a model of pyrogallol and in a model of hydrogen peroxide.