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.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
van Hoof HJ,Zijlstra FJ,Voss HP,Garrelds IM,Dormans JA,van Bree L,Bast Adoi
10.1080/09629359791497subject
Has Abstractpub_date
1997-01-01 00:00:00pages
355-61issue
5-6eissn
0962-9351issn
1466-1861journal_volume
6pub_type
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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journal_title:Mediators of inflammation
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