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Assessing mechanisms of immunotoxicity for polycyclic aromatic hydrocarbons in rainbow trout (Oncorhynchus mykiss)

During the past 30 years, numerous studies have focused on the toxicities of
polycyclic aromatic hydrocarbons (PAH). Laboratory and field studies have helped
elucidate the detrimental effects of these chemicals on growth, reproduction and
immune response. Polycyclic aromatic hydrocarbons are in the priority list of
chemicals to be studied by different governmental agencies and universities and
understanding their mechanisms of action is the focus of the current research. The
manuscripts presented in this dissertation are focused on the effects and mechanism of
action of PAH on disease susceptibility.
After a dietary exposure to PAH for up to 50 days (chapter II) and samplings after 3,
7, 14, 28 and 50 days, a number of biomarkers of PAH exposure were measured:
Fluorescent aromatic compounds (FACs) in bile, ethoxyresorufin-o-deethylase
(EROD) in liver microsomes, cytochrome P450 1A immunohistochemistry in liver
and kidney and adduct formation in liver. Additionally markers of oxidative stress
were measured: comet assay in blood, protein nitration in kidney and F2-isoprostanes
in kidney. Oxidative stress was a probable factor in PAH induced responses in fish adapted to long-term PAH exposures and aryl hydrocarbon activation was not
necessarily involved in this process. Disease challenge with Aeromonas salmonicida
(chapter III) resulted in differences in mortalities that demonstrated that fish exposed
to PAH were more susceptible to disease than fish not exposed to PAH. Determination
of gene expression in head kidney of fish exposed and not exposed to PAH challenged
with A. salmonicida using microarray and RT-PCR technologies 2, 4, 10 and 20 days
after challenge (chapter IV), suggested that PAH exposure was associated with down
regulation of interleukin 8, transport associated protein 1, NF-kB modulator,
recombination activating gene and major histocompatibility complex II two days after
challenge in fish exposed to PAH. The transcript levels were closer to control levels
20 days after challenge, this indicated a recovery from the effect of PAH exposure. / Graduation date: 2006

Identiferoai:union.ndltd.org:ORGSU/oai:ir.library.oregonstate.edu:1957/28873
Date09 December 2005
CreatorsBravo, Claudia F.
ContributorsCurtis, Lawrence R.
Source SetsOregon State University
Languageen_US
Detected LanguageEnglish
TypeThesis/Dissertation

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