A study of the coordination shell of aluminum(III) and magnesium(II) in model protein environments: Thermodynamics of the complex formation and metal exchange reactions

Protein Side Chains Facilitate Mg/Al Exchange in Model Protein Binding Sites

“…Finally, bond shortening has been observed on attachment of Al III to the binding site. [28,29] This was also addressed experimentally; it results in the loss of enzymatic activity. [9] Computational Methods All calculations were carried out with the Gaussian 98 [43] and Gaussian 03 [44] packages.…”

“…[28] Among the highest affinity ligands, acetate was found to be the strongest towards both cations, followed by methanethiol, methylimidazole, acetamide, and methanol. Combinations containing a methanethiol ligand were not pursued further since, even though they have favorable affinity, [28,29] they are not likely to be found in naturally occurring magnesium-binding sites. [27] Since the presence of one negatively charged carboxylate is ubiquitous for Mg II in naturally occurring protein binding sites in the PDB, [30] the next step was to study the coordination shell of both metals as formed by one acetate plus a second ligand chosen from the set of highest affinity ligands, namely, acetate, methylimidazole, acetamide, and methanol, as well as the water molecules required to complete the first coordination shell.…”

Understanding the cation specific effects on the aqueous solubility of amino acids: from mono to polyvalent cations

“…16,26,28,29 With the increasing bioavailability of this metal ion due to acid rain witnessed in the last decades, the study of the relationship between its levels in biological uids, and tissues and its potential involvement in neurological disorders, has gained a renewed interest. 25,27 In most natural systems, the aluminum absorption, excretion, tissue retention and deposition will depend on the properties of the Al 3+ complexes formed with biological ligands.…”

Molecular Basis of Aluminium Toxicity in Plants: A Review

“…Mg ion might be an important component of characterizing the physiology of Al resistance. Al 3+ toxicity may also provoke similar mitochondrial dysfunction [71] and ROS production in many plant species [72][73][74][75][76] presumably by causing Mg deficiency inside the mitochondria or by substituting Mg for Al 3+ in Mg 2+ -dependent enzymes [77,78]. Thus, mitochondrial Mg porters could be the target site for Al 3+ toxicity.…”