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Interactions between ultrafine particles and transition metals in vivo and in vitro.

Wilson, Martin R, Lightbody, Janet, Donaldson, Ken, Sales, Jill and Stone, Vicki (2002) Interactions between ultrafine particles and transition metals in vivo and in vitro. Toxicology and Applied Pharmacology, 184 (3). pp. 172-179. ISSN 0041-008X

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Abstract/Description

Both the ultrafine particle and transition metal components of particulate air pollution (PM10) have been hypothesized to be important factors in determining toxicity and potential adverse health effects. In this study we aimed to investigate interactions between transition metal salts and a surrogate environmental particle–ultrafine carbon black (ufCB). In all experimental systems employed, the ufCB was found to be more reactive than its fine counterpart (CB). Incubation of ufCB with the reactive oxygen species (ROS)-sensitive probe dichlorofluorescin in the absence of cells generated significantly more ROS than CB. With addition of either cupric sulfate (CuSO4), ferrous sulfate (FeSO4), or ferric chloride (FeCl3), the ROS generation in the presence of ufCB was enhanced in a potentiative manner. In Mono Mac 6 macrophages, ufCB again produced more ROS than CB. However, addition of iron salts had no additive effect over and above that induced in the macrophages by ufCB. In the mouse macrophage cell line J774, ufCB decreased the cellular content of GSH and ATP. Addition of iron further decreased both GSH and ATP and a potentiative interaction between ufCB and FeSO4 was observed, but only at the highest iron concentrations tested. A concentration-dependent increase in tumor necrosis factor- production by J774 cells was also observed following exposure to ufCB, which was not further enhanced by the addition of iron. J774 cells were also found to sequester or chelate iron without inducing toxicity. In the rat lung ufCB induced a significant neutrophil influx and this inflammatory effect was potentiativelly enhanced by the addition of FeCl3 (100 μM). These findings suggest that (1) ultrafine particles and metals interact by chemical potentiation in a cell-free environment to generate ROS, (2) potentiation between ultrafine particles and metal salts is not observed in the presence of macrophages as iron is sequestered or chelated by the cells, (3) in the lung, ultrafine particles and iron salts interact in a potentiative manner to generate inflammation.

Item Type: Article
Print ISSN: 0041-008X
Electronic ISSN: 1096-0333
Uncontrolled Keywords: Ultrafine; Transition metal; Oxidative stress; Carbon black; DCFH
University Divisions/Research Centres: Faculty of Health, Life & Social Sciences > School of Life Sciences
Dewey Decimal Subjects: 600 Technology > 610 Medicine & health > 612 Human physiology
600 Technology > 610 Medicine & health > 611 Human anatomy, cytology & histology
600 Technology > 610 Medicine & health > 614 Incidence & prevention of disease
Library of Congress Subjects: Q Science > QP Physiology
Item ID: 1630
Depositing User: RAE Import
Date Deposited: 05 Jun 2008 09:58
Last Modified: 17 Jun 2013 10:37
URI: http://researchrepository.napier.ac.uk/id/eprint/1630

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