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The present study explored the regulation and role of different AOEs during oxidative stress in human lung cells. Based on the results presented in this thesis, the main conclusions are:

  1. MnSOD is induced by TNF-α, but cytokine-induced MnSOD does not protect bronchial epithelial cells against endogenously or exogenously generated oxidants. In contrast, the cells with the highest MnSOD activity are those most sensitive to subsequent oxidant damage. The balance between various antioxidant enzymes, rather than the induction of one enzyme, is important for protecting cells during oxidant exposure.

  2. AOEs are not directly upregulated by high oxygen tension. Increases in the specific activities of AOEs and glutathione concentration are not necessary for the development of increased oxidant resistance in human bronchial epithelial cells.

  3. MnSOD is not induced by asbestos fibers alone in human mesothelial cells. Asbestos fibers and TNF treatments render these cells more vulnerable to oxidant-induced cell damage despite elevated MnSOD activity.

  4. Human alveolar macrophages scavenge exogenous H2O2 mainly by a catalase-dependent pathway, whereas the glutathione redox cycle is responsible for the maintenance of cellular integrity during the respiratory burst.

  5. Human inflammatory cells exhibit different antioxidant profiles. Monocytes have higher levels of glutathione and of enzymes of the GSH cycle, whereas in monocytes catalase activity is significantly lower than it is in neutrophils. The high catalase activity of neutrophils may explain their high resistance against exogenous H2O2, whereas low glutathione content and GSH-related enzymes may account for the poor survival of human neutrophils.

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