(598c) Antioxidant Protection from Oxidative Stress Damage in Human Pulmonary Cells

Exposure to pollutants and particulate matter cause oxidative stress through the direct introduction of exogenous ROS and compounds that drive free radical reactions, or indirectly through the recruitment and activation of inflammatory cells which release free radicals. The large surface area of the lungs and direct contact with inhaled air make the respiratory system highly susceptible to oxidative stress related injury, including DNA damage, cellular barrier dysfunction, and direct tissue damage. More susceptible populations include immunodeficient individuals, infants, elderly and those with pulmonary diseases such as asthma.

Previous groups have investigated the acute and subchronic exposure responses of human pulmonary cell line A549 to particulate exposure, including production of reactive oxygen species and cell viability. Antioxidant supplementation with Trolox, a commercially available vitamin E analog, has been investigated by various groups to decrease DNA damage and cell cycle arrest in A549s when acutely exposed to oxidants, including particulate matter (PM10). The first goal of this work was to characterize acute and chronic oxidative stress response parameters of the A549 cell line by the ratio of reduced and oxidized glutathione, chemokine production, DNA integrity, and surfactant secretion. The second goal was the development of an antioxidant formulation to prevent oxidative stress damage to the pulmonary cells.