Ascorbic acid modifies the surface of asbestos: possible implications in the molecular mechanisms of toxicity.

Ascorbic acid is one of the major components of the antioxidants defenses of the lung lining layer where inhaled asbestos fibers are deposited. Crocidolite fibers were incubated at 37 degrees C in a 0.01 M aqueous solution of ascorbic acid for 25 days in order to investigate modifications in surface reactivity. Iron (820 nmol/mg) and monomeric silica (470 nmol/mg) were released in the supernatant, while ascorbic acid was consumed. The amount of iron and silicon released, respectively, 17 and 6% (in atoms) of the total fiber content, exceeded what was expected at the surface, suggesting a partial disgregation of crocidolite promoted by ascorbic acid. In the absence of ascorbic acid but at the same pH, the release of iron and monomeric silica was minimal. At time intervals, aliquots of fibers were withdrawn to evidence chemical modifications progressively taking place. Three families of Fe(II) centers, differing in coordinative unsaturation and progressively removed during incubation, have been evidenced from the FTIR spectra of NO adsorbed onto the fibers. The most uncoordinated ones are removed first. New highly uncoordinated iron sites are exposed at the fiber surface as a consequence of the erosion of the outmost layers while hydration of silica tetrahedra yields new silanol groups. The activity in the Fenton-like reaction (*OH from H(2)O(2)) decreases following surface iron depauperation. Conversely, the homolytic cleavage of the C-H bond (CO(2)*-) from the formate ion) appears related to the small fraction of iron ions always present but easily quenched by the adsorption of ascorbic acid or its oxidation products.