title: Surface iron inhibits quartz-induced cytotoxic and inflammatory responses in alveolar macrophages.
abstract: The mechanism of enhancement/inhibition of quartz toxicity induced by iron is still unclear. Here the amount of iron on a fibrogenic quartz (Qz) was increased by wet impregnation (Fe(NO(3))(3) 0.67 and 6.7 wt %). X-ray diffraction (XRD), XRF diffuse reflectance, UV-vis, and infrared (IR) spectroscopies revealed dispersed ferric ions, and hematite aggregates at the higher loading. Surface features relevant to pathogenicity and cell responses were compared not only to the original quartz but also to reference quartz DQ12. Surface charge (ζ-potential) was more negative on the original and low-loaded specimen than on the high-loaded one. DQ12 had a less negative ζ-potential than Qz, ascribed to the absence of aluminium present in Qz (1.7 wt %). All quartz specimens were able to generate HO(•) radicals, iron-loaded samples being more reactive than original quartz. Iron deposition inhibited the rupture of a C-H bond. All quartzes were phagocytized by alveolar macrophages (AMΦ cell line NR8383) to the same extent, irrespective of their surface state. Conversely, iron loading increased AMΦ viability (evaluated by cytotoxicity and induction of apoptosis). Qz was found to be much less cytotoxic than DQ12. The induction of oxidative stress and inflammatory responses (evaluated by HO-1 mRNA expression and TNF-α mRNA and protein expression) revealed a reduction in inflammogenicity upon iron loading and a more inflammogenic potency of DQ12 ascribed to undissociated SiOH interacting via H-bonding with cell membrane components. The results suggest that besides aluminium also iron at the quartz surface may have an inhibitory effect on adverse health responses.
authors.affiliation: Dip. di Chimica IFM, G. Scansetti Interdepartmental Centre for Studies on Asbestos and Other Toxic Particulates, University of Torino, via Pietro Giuria 7, 10125 Torino, Italy.
authors.forename: Mara
authors.initials: M
authors.lastname: Ghiazza
authors.forename: Agnes M
authors.initials: AM
authors.lastname: Scherbart
authors.forename: Ivana
authors.initials: I
authors.lastname: Fenoglio
authors.forename: Francesca
authors.initials: F
authors.lastname: Grendene
authors.forename: Francesco
authors.initials: F
authors.lastname: Turci
authors.forename: Gianmario
authors.initials: G
authors.lastname: Martra
authors.forename: Catrin
authors.initials: C
authors.lastname: Albrecht
authors.forename: Roel P F
authors.initials: RP
authors.lastname: Schins
authors.forename: Bice
authors.initials: B
authors.lastname: Fubini
mesh_terms: D000535:Aluminum / Q000737:chemistry; D000818:Animals; D002460:Cell Line; D005290:Ferric Compounds / Q000737:chemistry* / Q000494:pharmacology; D005609:Free Radicals / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism; D006860:Hydrogen Bonding; D016676:Macrophages, Alveolar / Q000276:immunology / Q000378:metabolism*; D009566:Nitrates / Q000737:chemistry* / Q000494:pharmacology; D018384:Oxidative Stress; D011791:Quartz / Q000633:toxicity*; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D005290:Ferric Compounds; D005609:Free Radicals; D009566:Nitrates; D014409:Tumor Necrosis Factor-alpha; D011791:Quartz; D000535:Aluminum; D051547:Heme Oxygenase-1; C025302:ferric nitrate