Iron topochemistry and surface reactivity of amphibole asbestos: relations with in vitro toxicity.

Chemical reactivity of asbestos tremolite from Italy and USA localities and Union Internationale Contre le Cancer (UICC) crocidolite was studied in relation to Fe content, oxidation state, and structural coordination. Direct correlation between amount of Fe(2+) at the exposed M(1) and M(2) sites of the amphibole structure and fiber chemical reactivity was established. The in vitro toxicity of the same samples was investigated on human alveolar A549 cell line. Relationship between crystal-chemical features and cell toxicity is not straightforward. UICC crocidolite has Fe content and chemical reactivity largely higher than that of tremolite samples, but all show comparable in vitro toxic potential. Results obtained evidenced that Fe topochemistry is not a primary factor for induced cell toxicity, though it accounts for asbestos chemical reactivity (and possibly genotoxicity).

Spectroscopic and electrochemical study of the adsorption of [Co(en)2Cl2]Cl on gamma-alumina: influence of the alumina ligand on Co(III)/(II) redox potential.

UV-visible and Raman spectroscopies as well as electrochemical techniques have been used to characterize cis- and trans-[Co(III)(en)2Cl2]Cl (en=ethylenediamine) complexes and the gamma-alumina-supported cis-Co((III)) complex. It is shown that the electrochemical reduction of these complexes occurs according to a multistage mechanism involving two electrochemical steps, with the formation of a dimer that was characterized by UV-visible spectroscopy (intervalence band at 670 nm). The apparent standard redox potential for each step has been determined, and experimental results reveal that cis and trans complexes present similar electrochemical characteristics. It is also shown that the deposition of trans-[Co(III)(en)2Cl2]+ on gamma-alumina leads to an inner-sphere complex (ISC) in a cis configuration in which Cl- ligands are substituted by OH or O- surface groups of alumina. These changes in the coordination sphere of the complex induce a substantial decrease of its apparent redox potential since it is -0.63 V/SCE (saturated calomel electrode) for the gamma-alumina-supported cis-Co(III) complex, whereas values of -0.17 and -0.35 V/SCE were determined in dimethyl sulfoxide (DMSO) for the trans and cis precursor complexes, respectively.

Ferrous ion autoxidation and its chelation in iron-loaded human liver HepG2 cells.

Ferrous ion (Fe(2+)) is long thought to be the most likely active species, producing oxidants through interaction of Fe(2+) with oxygen (O(2)). Because current iron overload therapy uses only Fe(3+) chelators, such as desferrioxamine (DFO), we have tested a hypothesis that addition of a Fe(2+) chelator, 2,2'-dipyridyl (DP), may be more efficient and effective in preventing iron-induced oxidative damage in human liver HepG2 cells than DFO alone. Using ferrozine as an assay for iron measurement, levels of cellular iron in HepG2 cells treated with iron compounds correlated well with the extent of lipid peroxidation (r = 0.99 after log transformation). DP or DFO alone decreased levels of iron and lipid peroxidation in cells treated with iron. DFO + DP together had the most significant effect in preventing cells from lipid peroxidation but not as effective in decreasing overall iron levels in the cells. Using ESR spin trapping technique, we further tested factors that can affect oxidant-producing activity of Fe(2+) with dissolved O(2) in a cell-free system. Oxidant formation enhanced with increasing Fe(2+) concentrations and reached a maximum at 5 mM of Fe(2+). When the concentration of Fe(2+) was increased to 50 mM, the oxidant-producing activity of Fe(2+) sharply decreased to zero. The initial ratio of Fe(3+):Fe(2+) did not affect the oxidant producing activity of Fe(2+). However, an acidic pH (< 3.5) significantly slowed down the rate of the reaction. Our results suggest that reaction of Fe(2+) with O(2) is an important one for oxidant formation in biological system, and therefore, drugs capable of inhibiting redox activity of Fe(2+) should be considered in combination with a Fe(3+) chelator for iron overload chelation therapy.