Crystallite sizes and lattice parameters of nano-biomagnetite particles.

Average crystallite sizes of microbially synthesized pure, metal-, and lanthanide-substituted magnetite (bio-magnetite) were determined for a variety of incubation times and temperatures, substitutional elements and amounts, bacterial species, and precursor types. The intriguing difference between nanoparticle bio-magnetite and chemically synthesized magnetite (chem-magnetite) was that powder X-ray diffraction (XRD) data showed that the bio-magnetite exhibited slightly smaller lattice parameters, however, Raman Spectroscopy exhibited no difference in Fe-O bonding. These results indicate that bio-magnetite likely exhibits a more compact crystal structure with less uncoordinated iron on the surface suppressing negative pressure effects. The bio-magnetite with decreased lattice parameters could have potential technological advantages over current commercial chemically synthesized magnetites.

Hfe deficiency increases susceptibility to cardiotoxicity and exacerbates changes in iron metabolism induced by doxorubicin.

The clinical use of doxorubicin (DOX), an anthracycline chemotherapeutic agent, is limited by cardiotoxicity. The possible involvement of iron in DOX-induced cardiotoxicity became evident from studies in which iron chelators were shown to be cardioprotective. Iron overload is found in hereditary hemochromatosis, a genetic disorder prevalent in individuals of European descent. We hypothesized that Hfe deficiency may increase susceptibility to DOX-induced toxicity. Acute cardiotoxicity and iron changes were studied after treatment with DOX in Hfe knock-out (Hfe-/-) mice and wild-type mice. DOX-induced iron metabolism changes were intensified in Hfe-/- mice, which accumulated significantly more iron in the heart, liver, and pancreas, but less in the spleen compared with wild-type mice. In addition, Hfe-deficient mice exhibited significantly greater sensitivity to DOX-induced elevations in serum creatine kinase and aspartate aminotransferase. Increased mortality after chronic DOX treatment was observed in Hfe-/- mice and Hfe+/-mice compared with wild-type mice. DOX-treated Hfe-/- mice had a higher degree of mitochondrial damage and iron deposits in the heart than did wild-type mice. These data demonstrate that Hfe deficiency in mice increases susceptibility to DOX-induced cardiotoxicity and suggest that genetic mutations related to defects in iron metabolism may contribute to its cardiotoxicity in humans.