Beryllium and its compounds are highly toxic to most living cells, but the mechanisms of the interference with the biological substrates on the molecular level is not understood. From observations in (attempted) chemotherapy of beryllium poisoning using a variety of complexing agents it has been concluded that Be2+ is interacting predominantly with carboxyl as well as hydroxyl functions of protein bio-polymers, with complete deprotonation of the alkoxy or phenoxy functions involved. As a first support for this hypothesis, an analytically well-defined beryllium complex of glycolic acid has now been isolated from aqueous solutions under nearphysiological conditions, crystallized and its structure determined by X-ray diffraction. The hexanuclear complex features beryllium in two different environments, mono- and bis-chelated by glycolate ligands with deprotonated hydroxyl groups. In 9Be-NMR studies of aqueous solutions of the complex (pH 6) the persistence of complexation in two different environments of Be2+ could also be confirmed. The new structure may serve as a model for beryllium complexation with larger bio-ligands.
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Kumberger et al. (1992) studied this question.
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