Abstract 1790: Mutagenic effects of inorganic particulate matter on Raji and HepG2 cell lines exposed to ultraviolet radiation

Epidemiological studies have correlated exposure to ultraviolet-irradiated particulate matter with cardiovascular, respiratory, and malignant lung diseases. This study investigated the DNA damage induced by two major inorganic particulate matter compounds found in diesel exhaust, ammonium nitrate and ammonium sulfate on Burkitt's lymphoma (Raji) and hepatocellular carcinoma (HepG2) cell lines. We found a dose-dependent positive correlation of accumulated DNA damage in concentrations of ammonium nitrate and ammonium sulfate (25 μg/ml, 50 μg/ml, 100 μg/ml, 200 μg/ml, 400 μg/ml) with ultraviolet exposure (250 J/m2, 400 J/m2, 600 J/m2, 850 J/m2), as measured by the Comet Assay in both cell lines. There was a significant difference between the treated ammonium nitrate samples and negative control samples in Raji and HepG2 (p < 0.001). Apoptosis was shown in Raji and HepG2 cells when exposed to high concentrations of ammonium nitrate (200 μg/ml, 400 μg/ml) for 1 hour in samples without ultraviolet exposure, as assessed by the Comet Assay. However, the quantity of apoptotic cells greatly diminished after ultraviolet exposure at these concentrations. To further investigate and clarify the underlying mechanisms, we used Annexin V to quantify apoptosis. Flow Cytometry confirmed the results shown by the Comet Assay; ultraviolet exposure diminished apoptosis in ammonium nitrate-induced DNA damage in both Raji and HepG2. Ammonium sulfate induced DNA damage with or without ultraviolet influence was minimal as assessed by the Comet Assay in both cell lines, with a significant difference (p < 0.05) between the treated and negative control samples. These results indicate that the inorganic particulate compound, ammonium nitrate, induced DNA strand breaks at all concentrations and apoptosis at high concentrations in Raji and HepG2 cells, with ultraviolet radiation preventing apoptosis at high concentrations. We hypothesize that ultraviolet radiation inhibits an essential cellular mechanism, possibly involving p53, thereby explaining this phenomenon. Further studies are necessary to characterize the roles of apoptosis inhibition in DNA damage caused by inorganic particulate matter. Citation Format: Michael Xiao, Atif El-Naggar, Albert V. Helsing, Philip M. Lynch, Melissa M. Alegre, Richard A. Robison, Kim L. O'Neill. Mutagenic effects of inorganic particulate matter on Raji and HepG2 cell lines exposed to ultraviolet radiation. [abstract]. In: Proceedings of the 104th Annual