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Review Article Volume 13 Issue 4
Coordination chemistry as the governing principle of gadolinium biology: from GBCA design to dissociation, endogenous coordination, and chelation
Richard Semelka
Received: September 11, 2026 | Published: October 1, 2026
Citation: Semelka RC, Ramalho M. Coordination chemistry as the governing principle of gadolinium biology: from GBCA design to dissociation, endogenous coordination, and chelation. J Appl Biotechnol Bioeng. 2026;13(4):128-133. DOI: 10.15406/jabb.2026.13.00427
Abstract
Coordination chemistry provides a continuous molecular framework for gadolinium from the manufacture of a gadolinium-based contrast agent (GBCA) through biological retention, ligand exchange, endogenous re-coordination, and eventual chelation. A GBCA begins as a deliberately engineered Gd(III) coordination complex in which water accessibility, relaxivity, solubility, thermodynamic stability, kinetic inertness, distribution, and elimination must be balanced. If the original pharmaceutical coordination environment is disrupted, gadolinium does not become chemically undefined; it enters new coordination environments involving endogenous ligands. Phosphate-containing species have the strongest direct support as an inorganic binding environment for released Gd, while proteins, carbonate, other oxyanions, and mixed mineral-organic phases may also participate. Therapeutic chelation addresses the same coordination chemistry from the opposite direction. The chelator must reach retained Gd, compete with the existing coordination environment, form a sufficiently stable complex under physiological conditions, keep that complex soluble during transport, and permit elimination. Recent human data comparing four chelators illustrate why stability of a preformed complex alone does not establish in vivo performance. Paired urinary data demonstrate mobilization and increased excretion of an accessible Gd pool, but they do not identify its tissue or molecular origin, quantify total-body removal, or establish that retained Gd is causal for Gadolinium Deposition Disease (GDD). Clinical evidence for DTPA remains observational, and its use for GDD is off-label. This review develops accessibility as the connecting concept across the gadolinium molecular life cycle and presents DTPA- mediated decorporation as a mechanistically testable therapeutic approach requiring further controlled clinical evaluation.
Keywords: gadolinium, coordination chemistry, gadolinium-based contrast agents, DTPA, chelation, ligand exchange, phosphate, gadolinium retention, decorporation, accessibility
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