Fauré M, Lissi E A, Videla L A
Departamento de Química, Facultad de Ciencia, Universidad de Santiago, Chile.
Chem Biol Interact. 1991;77(2):173-85. doi: 10.1016/0009-2797(91)90072-f.
The antioxidant capacity of thyroid hormones and the antithyroid drug propylthiouracil was studied in three model systems, namely, autoxidation of rat brain homogenates and oxidation of rat erythrocyte plasma membranes (EPM) induced by either 2,2'-azobis-(2-amidinopropane) (AAP) thermolysis or by gamma irradiation. Thyroid hormones significantly inhibited the development of lipid peroxidation in these systems at micromolar concentrations, as assessed either by visible light emission, thiobarbituric acid reactive substances accumulation or oxygen uptake. This behaviour was not observed when L-3,3',5-triiodothyronine (T3) and L-thyroxine (T4) were assayed at nanomolar concentrations. In EPM exposed to AAP or gamma irradiation, propylthiouracil inhibited the induced lipid peroxidation, with Q1/2 values of 112-150 microM. It is concluded that the antioxidant capacity of thyroid hormones found in vitro may not be of relevance in physiological conditions, which exhibit variations of T3 and T4 levels in the nanomolar range. On the other hand, the behaviour of propylthiouracil as an inhibitor of EPM lipid peroxidation is observed at concentrations close to the therapeutic levels, thus representing a possible complementary action to its antithyroid activity.
在三个模型系统中研究了甲状腺激素和抗甲状腺药物丙硫氧嘧啶的抗氧化能力，即由2,2'-偶氮双-(2-脒基丙烷)(AAP)热解或γ射线照射诱导的大鼠脑匀浆自氧化和大鼠红细胞质膜(EPM)氧化。甲状腺激素在微摩尔浓度下能显著抑制这些系统中脂质过氧化的发展，这通过可见光发射、硫代巴比妥酸反应性物质积累或氧摄取来评估。当以纳摩尔浓度测定L-3,3',5-三碘甲状腺原氨酸(T3)和L-甲状腺素(T4)时，未观察到这种行为。在暴露于AAP或γ射线照射的EPM中，丙硫氧嘧啶抑制诱导的脂质过氧化，Q1/2值为112 - 150微摩尔。结论是，在体外发现的甲状腺激素的抗氧化能力在生理条件下可能不相关，因为生理条件下T3和T4水平在纳摩尔范围内变化。另一方面，在接近治疗水平的浓度下观察到丙硫氧嘧啶作为EPM脂质过氧化抑制剂的行为，因此这可能是其抗甲状腺活性的一种补充作用。
