Endocrine Abstracts (2008) 16 P366

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

Agnieszka Kokoszko1, Jan Dabrowski1, Janusz Szosland2, Andrzej Lewinski1 & Malgorzata Karbownik-Lewinska2


1Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Lodz, Poland; 2Department of Oncological Endocrinology, Medical University of Lodz, Lodz, Poland.


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.

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