Ferredoxins are small proteins containing iron and sulfur atoms organized as iron-sulfur clusters. These biological "capacitors" can accept or discharge electrons, the effect being change in the oxidation states (+2 or +3) of the iron atoms. This way, ferredoxin acts as electron transfer agents in biological redox reactions.
Adrenodoxin (adrenal ferredoxin; InterPro: IPR001055), putidaredoxin, and terpredoxin make up a family of soluble Fe2S2 proteins that act as single electron carriers, mainly found in eukaryotic mitochondria and Proteobacteria. The human variant of adrenodoxin is referred to as ferredoxin-1 and ferredoxin-2. In mitochondrial monooxygenase systems, adrenodoxin transfers an electron from NADPH:adrenodoxin reductase to membrane-bound cytochrome P450.
- Ferredoxin-1 in humans participates in the synthesis of thyroid hormones. It also transfers electrons from adrenodoxin reductase to CYP11A1, a CYP450 enzyme responsible for cholesterol side chain cleavage. FDX-1 has the capability to bind to metals and proteins.
- Ferredoxin-2 participates in heme A and iron–sulphur protein synthesis.
CHEMICAL STRUCTURE AND IMAGES
When relevant for the function
- Primary structure
- Secondary structure
- Tertiary structure
- Quaternary structure
Protein Aminoacids Percentage
SYNTHESIS AND TURNOVER
- Cell signaling and Ligand transport
- Structural proteins
With regard to (1), thyroidal ferredoxin and its NADPH-dependent reductase will be purified from thyroid particulate preparations and the structural and functional relationship of ferredoxin-reductase to flavoprotein iodotyrosine deiodinase will be studied.
Matched in Keywords: triiodothyronine .
Applying a systems approach to thyroid physiology: Looking at the whole with a mitochondrial perspective instead of judging single TSH values or why we should know more about mitochondria to understand metabolism. 2017
Classical thinking in endocrine physiology squeezes our diagnostic handling into a simple negative feedback mechanism with a controller and a controlled variable. In the case of the thyroid this is reduced to TSH and fT3 and fT4, respectively. The setting of this tight notion has no free space for any additions. In this paper we want to challenge this model of limited application by proposing a construct based on a systems approach departing from two basic considerations. In first place since the majority of cases of thyroid disease develop and appear during life it has to be considered as an acquired condition. In the second place, our experience with the reversibility of morphological changes makes the autoimmune theory inconsistent. While medical complexity can expand into the era of OMICS as well as into one where manipulations with the use of knock-outs and -ins are common in science, we have preferred to maintain a simple and practical approach. We will describe the interactions of iron, magnesium, zinc, selenium and coenzyme Q10 with the thyroid axis. The discourse will be then brought into the context of ovarian function, i.e. steroid hormone production. Finally the same elemental players will be presented in relation to the basic mitochondrial machinery that supports the endocrine. We propose that an intact mitochondrial function can guard the normal endocrine function of both the thyroid as well as of the ovarian axis. The basic elements required for this function appear to be magnesium and iron. In the case of the thyroid, magnesium-ATP acts in iodine uptake and the heme protein peroxidase in thyroid hormone synthesis. A similar biochemical process is found in steroid synthesis with cholesterol uptake being the initial energy-dependent step and later the heme protein ferredoxin 1 which is required for steroid synthesis. Magnesium plays a central role in determining the clinical picture associated with thyroid disease and is also involved in maintaining fertility. With the aid of 3D sonography patients needing selenium and/or coenzyme Q10 can be easily identified. By this we firmly believe that physicians should know more about basic biochemistry and the way it fits into mitochondrial function in order to understand metabolism. Contemplating only TSH is highly reductionistic.
Author's profiles and motivation for this analysis The philosophical alternatives in science and medicine Reductionism vs. systems approach in clinical thyroid disease guidelines The entry into complexity: the involvement of the musculoskeletal system Integrating East and West: teachings from Chinese Medicine and from evidence based medicine (EBM) Can a mathematical model represent complexity in the daily thyroid practice? How effective is thyroxine treatment? Resolving the situation of residual symptoms in treated patients with thyroid disease Importance of iron, zinc and magnesium in relation to thyroid function Putting together new concepts related to thyroid function for a systems approach Expanding our model into general aspects of medicine