Endocrine Abstracts

Iron participates in the Fenton reaction (Fe²⁺+H₂O₂+H⁺→Fe³⁺+^•OH+H₂O), the most basic reaction of oxidative stress. This transition metal is required to keep oxidative balance, although iron overload is associated with enhanced oxidative damage and cancer initiation. Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are also involved in oxidative processes, lipid peroxidation included.

The aim of the study was to evaluate the in vivo effect of GH, IGF-I and/or iron on lipid peroxidation in different rat tissues.

Male Wistar rats were administered iron as ferrous sulphate (FeSO₄; 3 mg/100 g b.w., on the 8th day of the experiment) and/or GH (0.2 IU/100 g b.w., once daily, for 8 days), and/or IGF-I (2 μg/100 g b.w., once daily, for 8 days). The level of lipid peroxidation products – malondialdehyde+4-hydroxyalkenals (MDA+4-HDA) – was measured spectrophotometrically in rat brain, lung, small intestine, liver, kidney, testis, spleen, and serum.

Among several examined tissues, only the small intestine and the brain appeared to be sensitive to oxidative effects of either GH, or IGF-I and/or iron.

Iron injection significantly increased lipid peroxidation only in the rat small intestine and that effect was completely prevented by either GH or IGF-I. In the rat brain, GH significantly decreased the basal lipid peroxidation, whereas IGF-I, either used alone or together with iron, significantly increased lipid peroxidation level.

In conclusion, not all rat tissues are equally sensitive to iron-induced lipid peroxidation, with only small intestine revealing such a property. GH and IGF-I possess some ability to prevent iron-induced oxidative damage in iron sensitive tissues, whereas contributing by themselves to oxidative imbalance in other tissues.