Trace elements: Selenium, Copper and Iodine

Mechanism

Specific molecular mechanisms

1. Selenium (Se) and Selenoproteins

Selenium is cotransductionally integrated into cellular proteins in the form of the modified amino acid selenocysteine, considered the twenty-first amino acid. Selenoproteins perform critical metabolic functions:

• Glutathione Peroxidase (GPx): Catalyzes the reduction of cellular hydrogen peroxide to harmless water molecules using reduced glutathione: H₂O₂ + 2GSH GPx (Selenium) 2H₂O + GSSG
• Iodothyronine Deiodinases (D1, D2, D3): Enzymes responsible for subtracting an iodine atom from the prohormone thyroxine (T₄) to convert it into the active hormone triiodothyronine (T₃) in target tissues.

2. Copper (Cu) and Metalloproteins

Copper acts inside metalloenzymes that coordinate the transfer of electrons, specifically binding to albumin for its initial transport. In the liver, it is incorporated into the glycoprotein ceruloplasmin, which acts in plasma as a ferroxidase, accelerating the oxidation of ferrous to ferric iron for transport. Likewise, copper is a cofactor of cytochrome c oxidase, the final complex of the mitochondrial electron transport chain.

3. Iodine (I) and Thyroid Hormonogenesis

Iodine actively taken up by the sodium-iodide symporter (NIS) in the basement membrane of thyrocytes is oxidized by thyroperoxidase (TPO) using hydrogen peroxide. It subsequently binds to tyrosyl residues of thyroglobulin in the colloidal lumen (organization), forming monoiodotyrosine (MIT) and diiodotyrosine (DIT), precursors of the thyroid hormones T₃ and T₄.

Wolff-Chaikoff and Jod-Basedow effect

Exposure to massive doses of iodine can provoke two antagonistic thyroid responses:

• Wolff-Chaikoff effect: Acute and transient blockade of the synthesis and release of thyroid hormones due to inhibition of thyroperoxidase induced by high intrathyroidal concentrations of iodine. It is used clinically with Lugol's solution to induce rapid remission of goiter before surgery.
• Jod-Basedow effect: Induction of severe hyperthyroidism in patients with multinodular goiter or latent thyroid autonomy after a sudden load of iodine that acts as a substrate for unregulated synthesis.

Indicators and dose

Clinical Indications and Organic Adjustment

Indicated for nutritional supplementation in prolonged total parenteral nutrition, endemic goiter (prevention of cretinism and childhood growth retardation) and hypothyroidism due to iodine deficiency.

Copper clearance is predominantly biliary, so in patients with severe hepatic cholestasis or obstructive cirrhosis, the dosage of copper in parenteral nutrition should be suspended or strictly reduced to prevent tissue accumulation and intoxication.