Effects of growth hormone and insulin-like growth factor-I on the iron-induced lipid peroxidation in the rat liver and porcine thyroid homogenates

OBJECTIVES: Growth hormone (GH) and its tissue mediator, insulin-like growth factor-I (IGF-I), are involved in oxidative processes, lipid peroxidation (LPO) included. Bivalent iron (Fe2+) is frequently used to experimentally induce oxidative damage to macromolecules (Fe2+ + H2O2 + H+ -> Fe3+ + (OH)-O-center dot + H2O). The aim of the study was to evaluate the effect of GH and/or IGF-I on the iron-induced LPO in the rat liver and porcine thyroid homogenates. METHODS: Rat liver and porcine thyroid homogenates were incubated in presence of GH (100; 10; 1.0; 0.1; 0.01; 0.001; 0.0001 mu g/ml) or IGF-I (1000; 100; 10; 1.0; 0.1; 0.01; 0.001; 0.0001 mu g/ml) or GH (100 mu g/ml) + IGF-I, or FeSO4 + H2O2 plus GH and/or IGF-I. The level of LPO was expressed as concentrations of malondialdehyde+4-hydroxyalkenals (MDA+4-HDA) per mg of protein. RESULTS: GH and/or IGF-I did not change the basal level of oxidative damage to lipids. In the rat liver homogenates, GH did not affect the iron-induced LPO, whereas IGF-I - in the lowest two concentrations - enhanced the process. In porcine thyroid homogenates, GH - in its two lowest concentrations - prevented, whereas in other concentrations, it enhanced the iron-induced LPO. IGF-I, in all used concentrations, enhanced the iron-induced LPO. CONCLUSION: GH and/or IGF-I may reveal prooxidative effects. This fact does not support their application in the treatment of disorders associated with increased oxidative damage.