The formation of ferruginous bodies is a good example of a biological problem that can benefit from the application of mineralogy and geochemistry. Ferruginous bodies are typically asbestos fibers that have become coated with an iron-rich material which is believed to be derived from proteins such as ferritin and hemosiderin [ Davis, 1970; Morgan and Holmes, 1985; Pooley, 1972]. Although ferruginous bodies were identified over 65 years ago [ Cooke, 1927; McDonald, 1927], relatively little is known about their formation. Gloyne [ Gloyne and Leeds, 1932] was unable to synthesize ferruginous bodies in various solutions (e.g., sulfuric and nitric acids, ferric chloride, sodium silicate, trypsin, bile, blood, and blood serum). However, it is now believed that the iron in the coating is derived from an Fe-bearing protein, which implies a synthesis mechanism different from those employed by Gloyne.
Several biological and mineralogical lines of evidence constrain the formation mechanism for ferruginous bodies. The ferruginous material consists of submicrometer ferrihydrite crystals, and similar-sized ferrihydrite crystals occur in the cores of ferritin and hemosiderin [ Treffry et al., 1987]. Ferruginous bodies are typically associated with agglomerations of macrophages (called giant cells) [ Koerten, 1990], implying that the macrophage has a role in the formation of ferruginous bodies. And, ferruginous bodies have characteristic morphologies [ Gloyne and Leeds, 1932] that appear to relate to the type of mineral at the core [ Kimizuka et al., 1988]. One morphological type is shown in Figure 1, in which the ferruginous coating is greatest at the fiber ends and at specific locations along the fiber. The association of morphology with mineral substrate and the preferential deposition at the ends of fibers suggest that the mineral substrate exerts some control over the formation of the ferruginous coating. The nature of this control is not known.
A possible mineralogical/geochemical mechanism that we are currently investigating is the denaturing of protein by minerals, perhaps via an oxidation/reduction process that occurs preferentially at fiber ends (i.e., at the ends of the amphibole fibers). Such oxidation/reduction reactions are known to occur preferentially in biotite at the edges of 2:1 layers [ Ilton et al., 1992] where electron transfer is presumably fastest. Furthermore, the mobilization of iron from ferritin can occur in the presence of a reducing agent [ Crichton, 1973]. Hence, mineral surfaces may be able to reduce ferritin, thereby causing it to release its iron core. We are attempting to synthesize ferruginous bodies in vitro using ferritin in aqueous solutions. We hypothesize that the mineral surface may be able to denature the protein directly; however, we are also investigating the potential role of hydrogen peroxide as a carrier of the charge from the mineral surface to the protein. (In vivo, hydrogen peroxide is released by macrophages, a cell type typically associated with ferruginous bodies.)