Date of Award
Master of Science (MS)
College of Science and Mathematics
Thesis Sponsor/Dissertation Chair/Project Chair
Ann Marie DiLorenzo
Not only did over 2,753 individuals perish on the morning of September 11, 2001, many have suffered from mental and physical illnesses ever since. Thousands of individuals experienced breathing complications, asthma and lung cancer. Clinical trials on cancer, including a patient who was exposed to the World Trade Center (WTC) dust, have seen a decrease in the progression of tumor growth with the use of oral nicotinamide adenine dinucleotide (NADH). NADH is naturally occurring within a cell’s mitochondria and aids in the production of adenosine triphosphate (ATP), the energy of the cell. NADH is an anti-aging, energy enhancing substance that also reduces fatigue and successfully treats degenerative medical conditions. NADH is becoming a possible treatment for tumor regression but it is still unknown, on a cellular level, the exact reason why NADH reacts with these cells to prevent further tumor growth. In this study, the amount of NADH produced by normal MRC-5 lung fibroblast cells will be compared to lung cells exposed to WTC dust, using a PROMEGA NAD+/NADH-Glo assay. The same cells will be evaluated to note the decline in the levels of Glutathione to determine the amount Reactive Oxidative Species (ROS) brought onto lung cells by WTC dust. ROS is known to decrease GSH levels by causing oxidative stress that leads to apoptosis. It is important for the cells to maintain high levels of reduced glutathione (GSH) and low levels of oxidized glutathione (GSSG). PROMEGA GSH Glo Glutathione assay will be used to determine if the toxic, mutagenic and apoptotic effects of WTC dust can be shown to be the result of oxidative stress. Lung fibroblast cells will be exposed to various concentrations of WTC dust, ranging from 25-250 parts per million (ppm). It is hypothesized that the cells with the highest concentrations of this toxic particulate matter will experience the most accumulation of oxidative stress, resulting in more NADH being oxidized to NAD+ within the mitochondria, and simultaneous decrease in protective antioxidants as shown in changes in the levels of reduced GSH. This should allow correlations to be made on a more precise cellular mechanism between exposure to this WTC dust, oxidative stress and loss of mitochondrial function seen in the diseases of the exposed first responder population.
Seder, Lara, "Increased Levels of Oxidative Stress in Human Fibroblast Lung Cell Cultures and the Loss of Mitochonndrial Function Due to Exposure to Particulate Matter from September 11, 2001" (2018). Theses, Dissertations and Culminating Projects. 150.