Title

Carbonaceous nanoparticle toxicity as a function of ferrous iron content

Document Type

Oral Presentation

Location

SURC Room 140

Start Date

15-5-2014

End Date

15-5-2014

Keywords

Nanoparticle, Carbon, Iron

Abstract

Experiments on mitochondria indicate that toxicity of inhalable atmospheric nanoparticles that are emitted from fossil fuel combustion correlates with both ferrous iron (Fe(II)) and anthracene concentrations in collected ultrafine particles (UFP). To further understand underlying chemical mechanisms responsible for this detrimental effect, UFPs and carbonaceous nanoparticles are investigated under simplified biological conditions while analyzing Fe(II) and the representative oxidative species hydrogen peroxide (H2O2). Realistic concentrations of Fe(II) at sub-nanomolar and H2O2 at nanomolar levels are quantified using flow injection analysis (FIA) with chemiluminescence. Results show that biological electron donors including ascorbate, glutathione, and NADPH when in the presence of black carbon (printex 90, flamruss 101, printex XE) generate H2O2. Under biological condition Fe(II) has a very short half-life, a matter of a few minutes. However when a large pool (1 μM) of redox active Fe(III) is added to solution an equilibrium is established between Fe(III) and Fe(II) with a small pool of Fe(II) remaining at a constant concentration in the pM range. When this pool of Fe(II) is present a reduction in H2O2 production is observed, it is well established that Fe(II) will react with H2O2 to generate hydroxyl radical. These results show that carbonaceous nanoparticles and iron are able to redox cycle and in the process generate reactive oxygen species in a catalytic manner that can raise havoc in biological systems (cardio, pulmonary diseases and cancer).

Faculty Mentor(s)

Johansen, Anne

Additional Mentoring Department

Chemistry

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May 15th, 3:40 PM May 15th, 4:00 PM

Carbonaceous nanoparticle toxicity as a function of ferrous iron content

SURC Room 140

Experiments on mitochondria indicate that toxicity of inhalable atmospheric nanoparticles that are emitted from fossil fuel combustion correlates with both ferrous iron (Fe(II)) and anthracene concentrations in collected ultrafine particles (UFP). To further understand underlying chemical mechanisms responsible for this detrimental effect, UFPs and carbonaceous nanoparticles are investigated under simplified biological conditions while analyzing Fe(II) and the representative oxidative species hydrogen peroxide (H2O2). Realistic concentrations of Fe(II) at sub-nanomolar and H2O2 at nanomolar levels are quantified using flow injection analysis (FIA) with chemiluminescence. Results show that biological electron donors including ascorbate, glutathione, and NADPH when in the presence of black carbon (printex 90, flamruss 101, printex XE) generate H2O2. Under biological condition Fe(II) has a very short half-life, a matter of a few minutes. However when a large pool (1 μM) of redox active Fe(III) is added to solution an equilibrium is established between Fe(III) and Fe(II) with a small pool of Fe(II) remaining at a constant concentration in the pM range. When this pool of Fe(II) is present a reduction in H2O2 production is observed, it is well established that Fe(II) will react with H2O2 to generate hydroxyl radical. These results show that carbonaceous nanoparticles and iron are able to redox cycle and in the process generate reactive oxygen species in a catalytic manner that can raise havoc in biological systems (cardio, pulmonary diseases and cancer).