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Risk of lung cancer in workers producing stainless steel and metallic alloys.

OBJECTIVES: The mortality of workers involved in the production of stainless and alloyed steel from 1968 to 1992 was studied, in order to investigate the risk of lung cancer due to exposure to metals, i.e. iron oxides, chromium and/or nickel compounds. METHODS: The study design was a historical cohort mortality study and a nested case-control study concerning lung cancer. Standardized mortality ratios (SMRs) were computed using regional mortality rates as an external reference for comparing observed and expected numbers of deaths, adjusting for age, sex and calendar time. Conditional logistic regression was used to estimate odds ratios (ORs). Occupational exposure was assessed through the complete job histories of cases and controls and a specific job-exposure matrix. RESULTS: The cohort comprised 4,288 male and 609 female workers. The observed overall mortality was significantly lower than expected [649 deaths; SMR = 0.91; 95% confidence interval (CI) 0.84-0.98]. No significant SMR was observed for mortality from lung cancer (54 deaths; SMR = 1.19; CI 0.88-1.55). The case-control study was based on 54 cases and 162 individually matched controls. Smoking habits were available for 71%. No lung cancer excess was observed for exposure to (1) metals and/or their compounds, i.e. iron (OR = 0.94, CI 0.48-1.86), chromium and/or nickel (OR = 1.18, CI 0.62-2.25), and cobalt (OR =0.64, CI 0.33-1.25), (2) acid mists (OR = 0.43, CI 0.17-1.10), and (3) asbestos (OR = 1.00, CI 0.54-1.86). With respect to exposure to polycyclic aromatic hydrocarbons (PAHs) and silica, which are often found together in workplaces, (1) high and statistically significant lung cancer excesses were observed, the ORs being 1.95 (CI 1.03-3.72) and 2.47 (CI 1.28-4.77) respectively, (2) quantitative exposure parameters revealed upward trends reaching statistical significance (P < 0.05), and (3) adjustments for tobacco consumption did not reveal any confounding factors from smoking. CONCLUSION: This study failed to detect any relationship between lung cancer and exposure to iron, chromium, nickel and/or their compounds. High and statistically significant relative risks, along with increasing trends, were observed for simultaneous exposure to PAHs and silica.

Aged↗

Aerobic ferrisiderophore reductase assay and activity stain for native polyacrylamide gels.

The reduction of ferric iron from microbial iron-binding compounds (siderophores) releases the iron from the siderophore so that it may be utilized by the microorganism. A method to detect aerobic ferrisiderophore reductase activity using ferrozine as a ferrous iron trap is shown to be applicable to cytoplasmic fractions from Rhodopseudomonas sphaeroides and four other different species of bacteria. The ferrisiderophore reductase uses reduced nicotinamide cofactors as reducing agents, and activity is stimulated by flavins. This assay has been adapted as a staining method to locate ferrisiderophore reductase activity in native polyacrylamide gels.

Aerobiosis↗

Nitric oxide donors modulate ferritin and protect endothelium from oxidative injury.

Ferritin protects endothelial cells from the damaging effects of iron-catalyzed oxidative injury. Regulation of ferritin occurs through the formation of an iron-sulfur cluster within a cytoplasmic protein, the iron regulatory protein (IRP) that controls ferritin mRNA translation. Nitric oxide has been shown to inhibit iron-sulfur proteins and is present at vascular sites of inflammation; therefore, we undertook a study to examine the influence of nitric oxide on changes in endothelial cell ferritin content in response to iron exposure, and the subsequent effects on susceptibility to oxidative injury. Iron-loaded endothelial cells (EC) exposed to nitric oxide donors synthesize markedly less ferritin. Treatment of EC with a nitric oxide donor increases IRP affinity for ferritin mRNA concomitant with a loss of cytoplasmic aconitase activity in iron-laden EC. Iron-treated EC exposed to NO donors were resistant to oxidative injury despite their low ferritin content when examined 1 h after the treatment period. In contrast, 24 h later, these same cells become sensitive to oxidants, whereas iron-treated EC that are ferritin-rich continue to be resistant. In conclusion, NO inhibits the increase of EC ferritin after exposure to iron but provides short-term protection against oxidants; ferritin, in turn, provides durable cytoprotection by inactivating reactive iron.

Aconitate Hydratase↗

Infrared spectroscopy of goethite dehydroxylation. II. Effect of aluminium substitution on the behaviour of hydroxyl units.

Dehydroxylation of goethite as affected by aluminium substitution was investigated using Fourier transform infrared spectroscopy (FT-IR) in conjunction with X-ray diffraction (XRD), thermogravimetric analysis (TGA) and differential thermogravimetric analysis (DTGA). The band intensities of hydroxyl vibrations were indicative of the degree of dehydroxylation and the changes in band parameters due to aluminium substitution were observed. The effect of aluminium substitution on band parameters of FT-IR spectra of goethite and its partially and fully dehydroxylated products, the mixture of goethite/hematite and hematite, were interpreted. The results of this study have confirmed that aluminium substituted goethite is thermally more stable than non-substituted goethite and is in harmony with the results of XRD and DTGA. A larger amount of non-stoichiometric hydroxyl units is associated with a higher aluminium substitution. A shift to a higher wavenumber of bending and hydroxyl stretching vibrations is attributed to the effects of aluminium substitution associated with non-stoichiometric hydroxyl units on the a-b plane relative to the b-c plane of goethite. The results provide information for the characterisation of activated bauxite containing hematite and goethite.

Aluminum↗

The hydrophilic phosphatriazaadamantane ligand in the development of H2 production electrocatalysts: iron hydrogenase model complexes.

As functional biomimics of the hydrogen-producing capability of the dinuclear active site in [Fe]H(2)ase, the Fe(I)Fe(I) organometallic complexes, (mu-pdt)[Fe(CO)(2)PTA](2), 1-PTA(2), (pdt = SCH(2)CH(2)CH(2)S; PTA = 1,3,5-triaza-7-phosphaadamantane), and (mu-pdt)[Fe(CO)(3)][Fe(CO)(2)PTA], 1-PTA, were synthesized and fully characterized. For comparison to the hydrophobic (mu-pdt)[Fe(CO)(2)(PMe(3))](2) and [(mu-H)(mu-pdt)[Fe(CO)(2)(PMe(3))](2)](+) analogues, electrochemical responses of 1-PTA(2) and 1-(PTA.H(+))(2) were recorded in acetonitrile and in acetonitrile/water mixtures in the absence and presence of acetic acid. The production of H(2) and the dependence of current on acid concentration indicated that the complexes were solution electrocatalysts that decreased over-voltage for H(+) reduction from HOAc in CH(3)CN by up to 600 mV. The most effective electrocatalyst is the asymmetric 1-PTA species, which promotes H(2) formation from HOAc (pK(a) in CH(3)CN = 22.6) at -1.4 V in CH(3)CN/H(2)O mixtures at the Fe(0)Fe(I) redox level. Functionalization of the PTA ligand via N-protonation or N-methylation, generating (mu-pdt)[Fe(CO)(2)(PTA-H(+))](2), 1-(PTA.H(+))(2), and (mu-pdt)[Fe(CO)(2)(PTA-CH(3)(+))](2), 1-(PTA-Me(+))(2), provided no obvious advantages for the electrocatalysis because in both cases the parent complex is reclaimed during one cycle under the electrochemical conditions and H(2) production catalysis develops from the neutral species. The order of proton/electron addition to the catalyst, i.e., the electrochemical mechanism, is dependent on the extent of P-donor ligand substitution and on the acid strength. Cyclic voltammetric curve-crossing phenomena was observed and analyzed in terms of the possible presence of an eta(2)-H(2)-Fe(II)Fe(I) species, derived from reduction of the Fe(I)Fe(I) parent complex to Fe(0)Fe(I) followed by uptake of two protons in an ECCE mechanism.

Adamantane↗

Synthesis of (-)-delobanone.

On irradiation in the presence of Fe(CO)(5) under a CO atmosphere, the alkenyl cyclopropane 2 underwent smooth ring expansion to give the sesquiterpene (-)-delobabone 3. The alkenyl cyclopropane 2 was prepared from the enantiomerically enriched epoxide 1.

Epoxy Compounds↗

Periodate modification of human serum transferrin Fe(III)-binding sites. Inhibition of carbonate insertion into Fe(III)- and Cu(II)-chelator-transferrin ternary complexes.

Periodate modification of human serum transferrin produces a species that binds Fe(III) weakly at pH 7.4 contrary to previous reports that Fe(III)-binding activity is completely lost. Ternary complexes of periodate-modified transferrin and either Fe(III) with nitrilotriacetate (NTA), oxalate, citrate, or EDTA, or of Cu(II) with oxalate could be formed. Peak wavelength maxima of these spectral bands are identical to those reported for native transferrin in the absence of bicarbonate. No carbonate ternary complexes of periodate-modified transferrin with Fe(III), Al(III), Cu(II), or Zn(II) could be formed. Conditional (Fe(NTA)) binding constants (log K) for C- and N-terminal modified sites are 7.33 and 7.54, respectively. The respective extinction coefficients at 470 nm are decreased 45% compared with the native protein. The electron paramagnetic resonance spectrum of the complex closely resembles that of the Fe(III)-NTA ternary complex formed with native transferrin in the absence of bicarbonate. Anions, including bicarbonate, at high concentrations destabilize formation of this Fe(III)-NTA ternary complex, while Fe(III) chelators readily remove the bound Fe(III). Bicarbonate, sulfate, and pyrophosphate still bind to the modified binding sites in the absence of metal although with slightly lower affinity and with lower molar difference absorptivities. Results are interpreted as an inhibition of a crucial protein conformational change by an intramolecular cross-link, preventing formation of the particularly stable metal-carbonate ternary complex from the less stable metal-chelate ternary complex. The method can be used to produce monosited transferrins.

Anions↗