4 Corrie Ct., Capalaba, QLD, 4157, Australia.
Eur J Clin Nutr. 2021 Aug;75(8):1170-1175. doi: 10.1038/s41430-020-00845-7. Epub 2021 Jan 29.
In the last few decades, there has been a resurgence in interest in the use of dietary supplements to treat diseases in humans and molybdenum has the potential to be used therapeutically. In humans, dietary molybdenum has been shown to treat iron-deficiency anemia and it may treat joint pain in arthritis. It has been proposed that the anti-anemic and tentative anti-arthritic properties of molybdenum are because it is increasing the activity of one or more mammalian molybdoenzymes. Molybdenum forms part of the active site of these enzymes. Despite this, it is unlikely that a molybdenum deficiency can develop in humans that are on an oral diet and not exposed to unsafe levels of a molybdenum antagonist. Therefore, the underlying mechanism by which dietary molybdenum treats or may treat these diseases is currently not known. This minireview examines three possible underlying mechanisms. It investigates the possibility that molybdenum: increases the quantity of active mammalian molybdoenzymes, restores or partially restores activity to malfunctioning mammalian molybdoenzymes, or blocks nuclear receptors, in cells. The examination of these mechanisms has provided an impression of the mechanism by which molybdenum treats iron-deficiency anemia and may treat arthritis; and hypothesize uses of molybdenum for other human diseases.
在过去的几十年中，人们对使用膳食补充剂来治疗人类疾病的兴趣再次高涨，而钼有可能被用于治疗。在人类中，膳食钼已被证明可治疗缺铁性贫血，并且可能治疗关节炎的关节痛。有人提出，钼的抗贫血和暂定抗关节炎特性是因为它增加了一种或多种哺乳动物钼酶的活性。钼是这些酶的活性部位的一部分。尽管如此，在饮食中摄入钼且未接触不安全水平的钼拮抗剂的情况下，人类不太可能出现钼缺乏症。因此，目前尚不清楚膳食钼治疗或可能治疗这些疾病的潜在机制。这篇综述探讨了三种可能的潜在机制。它研究了钼是否能够增加活性哺乳动物钼酶的数量、恢复或部分恢复功能失调的哺乳动物钼酶的活性、或阻断细胞中的核受体。对这些机制的研究提供了钼治疗缺铁性贫血和可能治疗关节炎的机制的印象；并假设钼可用于治疗其他人类疾病。
