Arthur J R, Beckett G J, Mitchell J H
Division of Micronutrient and Lipid Metabolism, Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK.
Nutr Res Rev. 1999 Jun;12(1):55-73. doi: 10.1079/095442299108728910.
Up to one billion people live in areas where they may be at risk from I deficiency. Many of the debilitating effects of the deficiency may be irreversible, consequently it is essential to understand the mechanisms whereby lack of I can cause disease through decreased thyroxine and 3, 3',5-triiodothyronine (T3) synthesis. Since Se has an essential role in thyroid hormone metabolism, it has the potential to play a major part in the outcome of I deficiency. These effects of Se derive from two aspects of its biological function. First, three Se-containing deiodinases regulate the synthesis and degradation of the biologically active thyroid hormone, T3. Second, selenoperoxidases and possibly thioredoxin reductase (EC 1.6.4.5) protect the thyroid gland from H2O2 produced during the synthesis of thyroid hormones. The mechanisms whereby Se deficiency exacerbates the hypothyroidism due to I deficiency have been elucidated in animals. In contrast to these adverse effects, concurrent Se deficiency may also cause changes in deiodinase activities which can protect the brain from low T3 concentrations in I deficiency. Animals with Se and I deficiency have changes in serum thyroid hormone concentrations that are similar to those observed in patients with I deficiency disease. However such animal models show no thyroid involution, a feature which is characteristic of myxoedematous cretinism in man. These observations imply that if Se deficiency is involved in the outcome of I deficiency in human populations it is likely that other interacting factors such as goitrogens are also implicated. Nevertheless the protection of the thyroid gland from H2O2 and the regulation of tissue T3 levels are the functions of Se that are most likely to underlie the interactions of Se and I.
多达10亿人生活在可能面临碘缺乏风险的地区。碘缺乏造成的许多使人衰弱的影响可能是不可逆转的，因此，了解碘缺乏通过甲状腺素和3,3',5-三碘甲腺原氨酸（T3）合成减少而导致疾病的机制至关重要。由于硒在甲状腺激素代谢中起重要作用，它有可能在碘缺乏的后果中发挥主要作用。硒的这些作用源于其生物学功能的两个方面。首先，三种含硒脱碘酶调节生物活性甲状腺激素T3的合成和降解。其次，硒过氧化物酶以及可能的硫氧还蛋白还原酶（EC 1.6.4.5）保护甲状腺免受甲状腺激素合成过程中产生的过氧化氢的侵害。在动物身上已经阐明了硒缺乏加剧碘缺乏所致甲状腺功能减退的机制。与这些不利影响相反，同时存在的硒缺乏也可能导致脱碘酶活性发生变化，从而保护大脑免受碘缺乏时低T3浓度的影响。硒和碘缺乏的动物血清甲状腺激素浓度的变化与碘缺乏病患者中观察到的变化相似。然而，这类动物模型没有甲状腺萎缩，而甲状腺萎缩是人类黏液水肿性克汀病的一个特征。这些观察结果表明，如果硒缺乏参与了人群中碘缺乏的后果，那么其他相互作用的因素如致甲状腺肿物质可能也有牵连。尽管如此，保护甲状腺免受过氧化氢的侵害以及调节组织T3水平是硒的功能，最有可能是硒与碘相互作用的基础。
