Endocrine Abstracts

Bivalent iron (Fe²⁺), which initiates the Fenton reaction (Fe²⁺+H₂O₂+H⁺→Fe³⁺+^•OH+H₂O), is frequently used to experimentally induce oxidative damage to macromolecules. Growth hormone (GH) and the main mediator of its action – insulin-like growth factor-I (IGF-I) – are involved in oxidative processes, lipid peroxidation (LPO) included.

The aim of the study was to evaluate the effect of GH and/or IGF-I on iron-induced LPO in rat liver and in porcine thyroid homogenates. In order to determine the effect of GH and/or IGF-I on basal LPO, the homogenates were incubated in the presence of GH (100, 10, 1.0, 0.1, 0.01, 0.001, 0.0001 μg/ml) or IGF-I (1000, 100, 10, 1.0, 0.1, 0.01, 0.001, 0.0001 μg/ml) or GH (100 μg/ml)+IGF-I. In order to study their effects on iron-induced LPO, the homogenates were incubated with FeSO₄ (15 μM or 40 μM, for the liver and for the thyroid, respectively)+H₂O₂ (0.1 mM or 0.5 mM, for the liver and for the thyroid, respectively) and, additionally, with GH and/or IGF-I. The level of LPO was expressed as the amount of malondialdehyde+4-hydroxyalkenals (MDA+4-HDA). GH and/or IGF-I did not affect basal LPO in either tissue. In rat liver homogenates, GH did not affect iron-induced LPO in any way, whereas IGF-I (0.001, 0.0001 μg/ml) enhanced the process. In porcine thyroid homogenates, GH, in its lowest two concentrations, completely prevented, whereas in other used concentrations, it enhanced iron-induced LPO. In turn, IGF-I, in all the used concentrations, enhanced iron-induced LPO in the porcine thyroid. In conclusion, GH and/or IGF-I may directly contribute to oxidative balance in the liver and in the thyroid under physiological conditions but, in case of induced oxidative stress, they may reveal prooxidative effects, which fact does not support their application in the treatment of disorders associated with increased oxidative damage.