Membrane lipids and nuclear DNA are differently susceptive to Fenton reaction substrates in porcine thyroid.

Fenton reaction (Fe(2+)+H(2)O(2) → Fe(3+)+()OH+OH(-)) is of special significance in the thyroid, as both substrates are indispensable for thyroid hormone synthesis, therefore being available presumably at high concentrations under physiological conditions. The study aimed at evaluation if both Fenton reaction substrates are required to induce oxidative damage to membrane lipids and nuclear DNA in porcine thyroid homogenates, and if these macromolecules are vulnerable to the same extent. Thyroid homogenates and nuclear DNA were incubated in the presence of H(2)O(2) and/or Fe(2+). Malondialdehyde+4-hydroxyalkenals (MDA+4-HDA) concentration (lipid peroxidation index) was measured spectrophotometrically, and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) concentration (DNA damage index) by HPLC. Whereas Fenton reaction substrates, used separately, did not affect lipid peroxidation, they increased 8-oxodG level for the highest H(2)O(2) concentration (100mM) and in Fe(2+) concentration-dependent manner (300, 150, 30 and 15 μM). If Fe(2+) and H(2)O(2) were applied together, lipid peroxidation increased significantly, however without H(2)O(2) concentration- but with clear Fe(2+) concentration-dependent effect. Concerning DNA damage, Fe(2+) enhanced H(2)O(2) effect, whereas Fe(2+) concentration-dependent effect was not changed by H(2)O(2). Excess of exclusively one of Fenton reaction substrates is sufficient to induce oxidative DNA damage, but not lipid peroxidation, in porcine thyroid. Comparing to H(2)O(2), Fe(2+) seems to be a stronger damaging substrate.