Epidemiologic studies indicate that for unknown reasons, living in cities with high levels of chemically complex carbon particulate increases asthmatic symptoms and the chances for a recurrent heart attack. To begin to determine the underlying biochemical mechanism, we synthetically produced representative pure carbon particles (particulate). Aerosol exposure to this particulate increases lung nitrotyrosine (NT) content in paraffin sections of mouse lungs-an observation suggesting increased oxidative stress since nitration of protein-bound tyrosine is the result of the interaction of protein bound tyrosines with peroxynitrate, a by-product of the interaction of superoxide anion with nitric oxide (NOx). We also found that NOx decreases in lavages of lungs of mice exposed to particulate aerosols containing 10 μg/m3 of carbon (a concentration occurring in the polluted cities) for 6 hours/day for 4 days. For this assessment, lungs were lavaged with saline, the cellular elements were removed by centrifugation, the supernatant was filtered through a filter with a pore size of 30,000 MW, and the filtrate concentration of nitrate/nitrite was assayed with a kit (Cayman Chem. Co. #780051). The sum of the nitrate and nitrite concentrations represents the total NOx. The average NOx concentrations of 4.2 μM of alveolar macrophages from the particulate exposed mice was significantly decreased (p < .05) compared with the average 5.4 μM levels of alveolar macrophages from non-particulate-exposed mice. In summary, exposure to air particulate decreases lung nitric oxide levels and increases lung nitrotyrosine concentrations in mice. These results are consistent with the possibility that following particulate exposure, lung NOx is used for peroxynitrate synthesis and nitrotyrosine formation. This oxidative reaction might contribute to the unexplained epidemiologic observations regarding the detrimental health effects of inhaling air pollutants in certain urban areas.
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