Fenton Reaction-Induced Oxidative Damage to Membrane Lipids and Protective Effects of 17β-Estradiol in Porcine Ovary and Thyroid Homogenates

The Fenton reaction (Fe(2+)+H(2)O(2)→Fe(3+)+(•)OH+OH(-)) results in strong oxidative damage to macromolecules when iron (Fe) or hydrogen peroxide (H(2)O(2)) are in excess. This study aims at comparing Fe(2+)+H(2)O(2)-induced oxidative damage to membrane lipids (lipid peroxidation, LPO) and protective effects of 17β-estradiol (a potential antioxidant) in porcine ovary and thyroid homogenates. Iron, as one of the Fenton reaction substrates, was used in the highest achievable concentrations. Thyroid or ovary homogenates were incubated in the presence of: (1st) FeSO(4)+H(2)O(2) with/without 17β-estradiol (1 mM; 100, 10.0, 1.0 µM; 100, 10.0, 1.0 nM; 100, 10.0, 1.0 pM); five experiments were performed with different FeSO(4) concentrations (2400, 1200, 600, 300, 150 µM); (2nd) FeSO(4) (2400, 1200, 600, 300, 150 µM)+H(2)O(2) with/without 17β-estradiol; three experiments were performed with three highest 17β-estradiol concentrations; (3rd) FeSO(4) (2400, 1200, 1100, 1000, 900, 800, 700, 600, 300, 150, 75 µM)+H(2)O(2) (5 mM). LPO level [MDA+4-HDA/mg protein] was measured spectrophotometrically. The basal LPO level is lower in ovary than in thyroid homogenates. However, experimentally-induced LPO was higher in the former tissue, which was confirmed for the three highest Fe(2+) concentrations (2400, 1200, 1100 µM). Exogenous 17β-estradiol (1 mM, 100, and 10 µM) reduced experimentally-induced LPO independently of iron concentration and that protective effect did not differ between tissues. The ovary, compared to the thyroid, reveals higher sensitivity to prooxidative effects of iron, however, it showed similar responsivity to protective 17β-estradiol activity. The therapeutic effect of 17β-estradiol against iron overload consequences should be considered with relation to both tissues.