All ETDs from UAB

Advisory Committee Chair

Shannon M Bailey

Advisory Committee Members

Dale A Dickinson

Michelle V Fanucchi

Document Type

Thesis

Date of Award

2012

Degree Name by School

Master of Science in Public Health (MSPH) School of Public Health

Abstract

Ozone (O3) is a primary component of photochemical smog and represents a serious public health concern as more than 50% of the U.S. population lives in areas exceeding national ambient air quality standards for this toxic pollutant. Recent findings indicate that the effects of inhaled O3 extend to extra-pulmonary tissues like the heart and liver. We hypothesize that inhaled O3 exposure-related events in the lung will cause downstream alterations in the liver proteome. To test this, we exposed male Sprague-Dawley rats to 0.5 ppm ozone for 8 hr a day for 5 days. After exposures, livers were removed and proteomic studies were performed. Histopathology and serum liver enzyme measurements showed that 5 day O3 exposure did not cause overt liver injury. Proteomic and mass spectrometry analysis successfully identified 10 proteins that were significantly altered, with 8 proteins increased and 2 decreased in abundance, as a consequence of O3 exposure. Importantly, several stress-induced proteins were significantly changed in response to O3; Grp78 and protein disulfide isomerase increased, whereas glutathione-S-transferase significantly decreased. No significant changes were detected when measuring the protein content of HO-1 and cytochrome P450s 2E1 and 2B as compared to control. Additionally, no significant lung injury was detected as measured by inflammatory cells and protein content in bronchoalveolar lavage fluid. In summary, these results suggest that an environmentally-relevant exposure to O3 modifies the liver proteome by altering key stress proteins in the liver. We propose that O3 and other inhaled pollutants may represent important unrecognized risk factors for exacerbating liver diseases.

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