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Cytotoxicity of Urban Dust and Diesel Exhaust Particulates in Murine Astrocyte Cells
Author(s) -
Fortuna Tyler R,
Price Peyton C,
Lopez Kevin J,
Schwader Andrew J,
Mazzer Paula
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.928.5
Subject(s) - oxidative stress , diesel exhaust , particulates , astrocyte , apoptosis , cytotoxicity , chemistry , population , environmental chemistry , toxicology , biology , diesel fuel , medicine , in vitro , biochemistry , environmental health , endocrinology , central nervous system , organic chemistry
Alzheimer's and related neurodegenerative diseases affect as many as 24 million individuals world‐wide—a number which will increase with our increasing global population. In a recent survey of epidemiological evidence, a panel of experts concluded that the existing data suggest a lower incidence of age‐related dementia in developing regions. A potential link between urban environments and neurodegenerative diseases was found by a series of studies conducted in dogs and humans in Mexico City, Mexico, which found markers of amyloid‐β accumulation and oxidative stress in their brains. Dogs and humans from rural areas did not show these neuropathological findings. These findings suggest that the difference may be due to the heavy airborne particular matter in Mexico City. We studied the ability of urban dust (NIST SRM 1649a) and diesel exhaust particulate matter (NIST SRM 2975) to induce cytotoxicity and oxidative stress in murine astrocyte cells (ATCC C8‐D1A). Diesel exhaust particulate matter (DEP) and urban dust (UD) have very different organic components, with UD containing a higher concentration of oxidized aromatic compounds. Therefore we hypothesized that these two airborne particulate types would produce different toxicological effects in our astrocyte cells. LC 50 determinations showed DEP to be more toxic with an LC 50 of 35μg/mL versus the LC 50 of UD at 52μg/mL. A caspase 3 activity assay showed that the enzyme was activated by DEP but not by UD. These data suggest that DEP is inducing apoptotic cell death while UD is inducing necrotic cell death. The difference in cell death suggests that UD could potentially be more harmful in vivo due to the release of intracellular components caused by the rupture of the cell membrane. The necrotic cell death could lead to the oxidative stress found in previous studies of brains form polluted environments. Support or Funding Information This work was sponsored by an Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant number P20GM103443.