Antioxidant or pro-oxidant properties of epinephrine (EPI) and isoprenaline (ISO) were studied in the absence and presence of Fe2+ , Fe3+ and Cu2+ ions. EPI and ISO (>2 /tmol/1) inhibited peroxidation of low density lipoprotein (LDL) induced by 2, 2’-azobis(2-amidino-propane) (AAPH). EPI had a similar inhibitory potency as ISO, but their potency was several times higher than the potency of a-tocopherol (a-TOC). When the LDL peroxidation was induced by 5 /tmol/1 CUSO4, EPI and ISO enhanced LDL peroxidation at low concentrations (10/mol/l) and decreased peroxidation at higher concentrations (30 /tmol/1). The compounds had a similar tendency to inhibit the peroxidation of phosphatidylcholine liposomes. EPI (3-30 //¿mol/1) inhibited lipid peroxidation of phosphatidylcholine liposomes induced by 2 mmol/1 of AAPH, but it was less effective and even increased the peroxidation, when the samples contained 2 mmol/1 AAPH with 50 /¿mol/l FeSC>4 or 2 mmol/1 AAPH with 20/imol/l FeCb. Inhibition of lipid peroxidation by EPI was also observed when studying decreased oxygen consumption, when the peroxidation of linoleic acid was induced by lipoxidase. In conclusion, EPI and ISO reduced lipid peroxidation, but they exhibit pro-oxidant properties in the presence of Fe2+, Fe3+ or Cu2+ ions, depending on the catecholamine and ionic concentration.
Certain liver metabolic diseases point to the presence of disturbances in glycogen deposition. Epinephrine raises the cAMP level that activates protein kinase A leading to the activation of phosphorylase and glycogen breakdown. In the present report, we sought to investigate whether NO is produced during adrenoceptor agonist-induced glycogenolysis in rat hepatocytes in cultures. Isolated glycogen rich rat hepatocytes in cultures were used. NO production (NO2-) was assessed under the effect of adrenergic agonists and adrenergic agonist/antagonist pairs, dibutyryl cyclic AMP sodium-potassium salt (db-cAMP), NO synthase (NOS) inhibitors Nω-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG) and the NO donor S-nitroso-N-acetyl penicillamine (SNAP) . The inducible NO synthase (iNOS) mRNA was examined by the reverse transcription-polymerase chain reaction (RT-PCR). Glycogenolysis was quantified by glucose levels released into medium. The amount of glucose and NO2- released by hepatocytes was increased as a result of epinephrine, phenylephrine or db-cAMP treatments. The increase in glucose and NO2- released by epinephrine or phenylephrine was blocked or reduced by prazosin pretreatment and by NOS inhibitors aminoguanidine and L-NAME. iNOS gene expression was up-regulated by epinephrine. It can be concluded that glycogenolysis occurs through α adrenoceptor stimulation and a signaling cascade may involve NO production., J. Hodis, N. Kutinová-Canová, P. Potměšil, L. Kameníková, E. Kmoníčková, Z. Zídek, H. Farghali., and Obsahuje biblografii a bibliografické odkazy