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Increased Lipid Peroxidation and Decreased Antioxidants in Lungs of Guinea Pigs Following an Allergic Pulmonary Response

Oxygen-derived radicals and cytokines are known to play key roles in cellular inflammation accompanying allergic lung disease. Using a well-characterized guinea pig model of pulmonary ovalbumin (OA) hypersensitivity, we studied lipid peroxidation and endogenous antioxidant reserve in bronchoalveolar...

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Bibliographic Details
Published in:Toxicology and applied pharmacology 1995-05, Vol.132 (1), p.72-81
Main Authors: Shvedova, A.A., Kisin, E.R., Kagan, V.E., Karol, M.H.
Format: Article
Language:English
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Summary:Oxygen-derived radicals and cytokines are known to play key roles in cellular inflammation accompanying allergic lung disease. Using a well-characterized guinea pig model of pulmonary ovalbumin (OA) hypersensitivity, we studied lipid peroxidation and endogenous antioxidant reserve in bronchoalveolar lung fluid (BAL) following a severe pulmonary allergic reaction. Since TNF-α is known to be involved in oxygen radical generation, we also examined TNF production in response to antigen challenge. By 24 hr after antigen challenge, the number of eosinophils in BAL was increased 3.5-fold compared with nonsensitized but challenged control animals. Immunohistochemical evaluation of BAL cells, employing a polyclonal antibody to murine TNF-α, demonstrated the presence of TNF in eosinophils. A 2.4-fold higher concentration of lipid peroxidation products was found in BAL fluid of sensitized and challenged vs nonsensitized, challenged guinea pigs (p < 0.05). Endogenous antioxidant levels were lower in the BAL fluid of the sensitized, challenged guinea pigs. The concentration of the major lipid-soluble antioxidant, vitamin E, was 8.7-fold lower than that in nonsensitized controls (p < 0.001) and the endogenous reserve of water-soluble antioxidants (thiols and ascorbic acid) was decreased 4-fold from that of control animals (p < 0.02). These results indicate an antioxidant/prooxidant imbalance associated with an allergic pulmonary episode.
ISSN:0041-008X
1096-0333
DOI:10.1006/taap.1995.1088