The aging phenomena is a process to which all organisms eventually succumb. The universality of this phenomena suggests that there may be one overwhelming factor involved. The exact biochemical basis of aging is still unclear. Free radicals such as the superoxide radical (O₂⁻) and the hydroxyl radical (OH⁻), formed in biological oxidation reactions may be responsible for cellular aging. Because of the high reactivity of the O₂⁻ and the OH⁻ they can produce extensive damage to lipids, proteins, and nucleic acids. In this study we have developed an <i>in vitro</i> quiescent model using density dependent bovine embryonic lung fibroblast (BELF). The effect of this process on the antioxidant defense enzymes such as, the superoxide dismutases, catalase, glutathione reductase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase, was studied. We have also extensively monitored the levels of free radical in the cell by both direct and indirect methods. The results indicate that no significant (p<0.05) changes in the activity of any of the major antioxidant enzymes in our quiescent model. Significant increases were observed in the intracellular levels of lipofuscin (age pigment) with time, but no changes in the generation of free radicals were observed using electron spin resonance spectrometry, cytochrome <i>c</i> reduction or spectrofluorometric techniques (caution should be placed in statistical interpretation of the data because of the small sample size in some experiments). The transcriptional and translational controls of the one of the major antioxidant defense enzymes (manganese superoxide dismutase) in bovine embryonic lung fibroblasts, human pulmonary artery endothelial cells (HPAE) and bovine PAE cell lines were also studied. Our preliminary data suggest that inhibitors of protein and RNA synthesis both cause a significant decrease in the induction of the manganese SOD in bovine pulmonary endothelial cells. / Master of Science