Joanne P. Marsh

TL;DR: The data indicate that epithelial cells of the respiratory tract respond to different oxidant insults by selective induction of certain antioxidant enzymes, and gene expression of antioxidant enzymes does not appear to be coordinately regulated in these cell types.

TL;DR: A novel method of chronic administration of antioxidant enzymes was developed to determine if lung injury, inflammation, and asbestosis could be inhibited in vivo in a rapid-onset, inhalation model of disease, and inactivated PEG-catalase failed to boost serum levels of catalase and did not inhibit asbestos-induced elevation of hydroxyproline in lung.

TL;DR: The data indicate that the profiles of AOE are dissimilar during the development of experimental asbestosis or silicosis and suggest different mechanisms of lung defense in response to these minerals.

TL;DR: A compendium of experimental results reported by this laboratory and others supports the hypothesis that scavengers of reactive oxygen metabolites and iron chelators prevent cytotoxicity after addition of asbestos to a variety of cell lines and macrophages in vitro.

TL;DR: Results above suggest asbestos-induced cell damage is mediated by active oxygen species, and the iron associated with the fiber and/or its interaction with cell membranes might be critical in driving a modified Haber-Weiss (Fenton-type) reaction resulting in production of OH.