MINERAL-MEDIATED DEGRADATIONS OF AMINO ACIDS

Recently, certain earth minerals have been shown to breakdown organic materials through processes of oxidation-reduction chemistry via surface reactions or formation of reactive oxygen species related to metals dissolution from the surfaces. In particular, iron sulfide (pyrite) and several forms of manganese oxides have been tested for their ability to degrade a number of amino acids, with the goal of understanding the mechanisms that could lead to mineral-mediated damage to proteins or DNA in the human body. Physiological systems such as the lungs are particularly vulnerable, where iron sulfide and manganese oxide dust can become trapped in the deep alveolar sacs. Other work has shown responses of macrophage cells from lung tissues when exposed to such minerals, indicating oxidative stress and potentially production of hydroxyl radicals. Determining mechanistic controls of mineral-mediated transformations of biomolecules is of central importance, and varies among minerals tested. Pyrite has been shown to produce hydroxyl radicals via the Fenton reaction at low pH brought about by dissolution of reduced sulfur to produce sulfuric acid in situ. Resulting products, which themselves degrade over time, include ortho-, meta-, and para-tyrosine at near equal-molar concentrations. The activity of the pyrite persists for several days, eventually decreasing in activity. Of four manganese oxides that have been tested, only Mn₂O₃ and MnO₂ have degraded phenylalanine in pure, unbuffered water; though the mechanism is still unclear as the products are not representative of hydroxyl radical attack. Use of model systems for solutions of humic, saline, and biological systems have also been examined for their role in the oxidation-reduction chemistry of the minerals. Phenylalanine hydroxylation in the presence of pyrite still occurs at appreciable rates in the presence of high levels of glycine, humic acids, and saline solution. However, there is competition in those solutions either for reaction with hydroxyl radical in solution or for active sites on the mineral surface. Degradation has been very limited in the simulated lung fluid, and the tyrosine oxidation products are not apparent; identification of unknown products and controls on important mechanisms are currently under investigation.