This paper reports on the effect of the Allende meteorite on the integrity of biological material and addresses the question whether it can induce cell damage via oxidative stress and cell mortality. The reaction mechanisms addressed herein are studied using electron-paramagnetic resonance spectroscopy (EPR), high-resolution transmission electron microscopy, scanning electron microscopy and energy dispersive spectroscopy, high-resolution X-ray diffraction, and the assays for thiobarbituric acid reactive substances (TBARS) and cell viability using 3-(4,5)-dimethylthiazol-2-yel-2,5-diphenyltetrazolium bromide (MTT bromide). As determined by the TBARS assay, Allende specimens induced cell damage via oxidative stress. The contents of TBARS in suspensions containing 1000 ppm of Allende and Fe1–xS were 6.8 ± 0.7 and 5.8 ± 0.6 nmol/mg protein, respectively. EPR experiments conducted on reaction mixtures containing Allende, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), and H2O2 showed a quartet signal, a 1:2:2:1 intensity, and hyperfine coupling constants corresponding to aN = 1.49 mT and aH = 1.49 mT, a signature of the DMPO-OH adduct. The intensity of the signal depended on the concentration of the solids in suspension, while the formation of DMPO-OH was limited by H2O2.
Experiments were conducted to test for the production of the DMPO-OH adduct from ferric ions, and the plausible generation of HO•. The role of ethanol (CH3CH2OH) as scavenger of HO• in Allende-DMPO suspensions was addressed. Results showed a six-line spectra, with hyperfine coupling constants aN = 15.8 G, aH = 22.6 G, and g = 2.0059, consistent with the formation of the DMPO-CH(OH)-CH3 adduct, but not DMPO-OCH2CH3. We explain these findings as the result of formation of HO• onto (or in proximity to) the mineral surface, with CH3CH2OH competing with DMPO for HO∞, and ferric iron playing a lesser role in DMPO transformation. Our findings are congruent with reported radical-scavenging experiments for pyrite under anoxic conditions, concluding the formation of HO∞ at surface defect sites.
Experiments conducted in Allende–desferrioxamine B(DFO-B) suspensions showed the inhibition of the formation of HO•, by means of decreases in the DMPO-OH adduct signal, accounted for by the reaction between Fe(II) and HO• to form Fe(III) and competing reaction mechanisms at the structural Fe centers, confirming that the production of HO∞ radicals is associated with iron centers and contributes to mineral dissolution. Small-sized magnetite domains present were recognized as catalytic sites for the production of HO∞ radicals. The γ-Fe3O4 domains present in the Allende matrix exhibited a submicron range, an elongated-hexagonal habit, and a high degree of crystallinity, supporting the presence of biogenic γ-Fe3O4. Cell viability was found to be susceptible to the distribution and atomic environment of structural Fe.