气候变化领域集成服务门户

Functional groups on the surface of fibrous silicates can complex iron. We tested the postulate that (1) asbestos complexes and sequesters host cell iron resulting in a disruption of metal homeostasis and (2) this loss of essential metal results in an oxidative stress and biological effect in respiratory epithelial cells. Exposure of BEAS-2B cells to 50 mu g/mL chrysotile resulted in diminished concentrations of mitochondrial iron. Preincubation of these cells with 200 mu M ferric ammonium citrate (FAC) prevented significant mitochondrial iron loss following the same exposure. The host response to chrysotile included increased expression of the importer divalent metal transporter-1 (DMT1) supporting a functional iron deficiency. Incubation of BEAS-2B cells with both 200 mu M FAC and 50 mu g/mL chrysotile was associated with a greater cell accumulation of iron relative to either iron or chrysotile alone reflecting increased import to correct metal deficiency immediately following fiber exposure. Cellular oxidant generation was elevated after chrysotile exposure and this signal was diminished by co-incubation with 200 mu M FAC. Similarly, exposure of BEAS-2B cells to 50 mu g/mL chrysotile was associated with release of the proinflammatory mediators interleukin (IL)-6 and IL-8, and these changes were diminished by co-incubation with 200 mu M FAC. We conclude that (1) the biological response following exposure to chrysotile is associated with complexation and sequestration of cell iron and (2) increasing available iron in the cell diminished the effects of asbestos exposure.