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van Hoof HJ, Zijlstra FJ, Voss HP, et al. The effect of ozone exposure on the release of eicosanoids in guinea-pig BAL fluid in relation to cellular damage and inflammation. Mediators Inflamm. 1997;6(5):355-61doi: 10.1080/09629359791497.
van Hoof, H. J., Zijlstra, F. J., Voss, H. P., Garrelds, I. M., Dormans, J. A., van Bree, L., & Bast, A. (1997). The effect of ozone exposure on the release of eicosanoids in guinea-pig BAL fluid in relation to cellular damage and inflammation. Mediators of inflammation, 6(5), 355-61. https://doi.org/10.1080/09629359791497
van Hoof, H J, et al. "The effect of ozone exposure on the release of eicosanoids in guinea-pig BAL fluid in relation to cellular damage and inflammation." Mediators of inflammation vol. 6,5 (1997): 355-61. doi: https://doi.org/10.1080/09629359791497
van Hoof HJ, Zijlstra FJ, Voss HP, Garrelds IM, Dormans JA, van Bree L, Bast A. The effect of ozone exposure on the release of eicosanoids in guinea-pig BAL fluid in relation to cellular damage and inflammation. Mediators Inflamm. 1997;6(5):355-61. doi: 10.1080/09629359791497. PMID: 18472870; PMCID: PMC2365875.
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Mediators Inflamm. 1997;6(5):355-61. doi: 10.1080/09629359791497.

The effect of ozone exposure on the release of eicosanoids in guinea-pig BAL fluid in relation to cellular damage and inflammation.

Mediators of inflammation

H J van Hoof, F J Zijlstra, H P Voss, I M Garrelds, J A Dormans, L van Bree, A Bast

Affiliations

  1. Leiden/Amsterdam Center for Drug Research, Department of Pharmacochemistry, Vrije Universiteit, De Boelelaan 1083, Amsterdam 1081 HV, The Netherlands. [email protected]

PMID: 18472870 PMCID: PMC2365875 DOI: 10.1080/09629359791497

Abstract

The observed effects after ozone exposure strongly depend on ozone concentration and exposure time. We hypothesized that depending on the O3 exposure protocol, mainly either an oxidant damage or an inflammation will determine the O3 toxicity. We compared two different ozone exposure protocols: an acute exposure (3 ppm 2 h) for studying the oxidant damage and an exposure (1 ppm 12 h) where an inflammatory component is also probably involved. We measured LDH activity and protein and albumin exudation as markers for cellular damage. After the acute exposure an increase in LDH activity was measured and after exposure to 1 ppm ozone for 12 h the exudation of protein and albumin was also enhanced. The histological examinations showed a neutrophilic inflammatory response only after exposure to 1 ppm ozone for 12 h. The acute exposure protocol resulted in an increased release of PGE2, PGD2, PGF2alpha and 6-ketoPGF1alpha whereas exposure to 1 ppm ozone for 12 h led to an additional release of LTB4. No effects were measured on the release of TxB2 and LTC4/D4/E4. These changed amounts of eicosanoids will probably contribute to the ozone-induced lung function changes.

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