Biomarker responses and disease susceptibility in juvenile rainbow trout Oncorhynchus mykiss fed a high molecular weight PAH mixture

Abstract

Juvenile rainbow trout were fed a diet containing an environmentally relevant mixture of 10 high molecular weight polycyclic aromatic hydrocarbons (PAHs) at a dose of 0.66 or 7.82 µg PAH · g fish(-1) · d(-1). At 3, 7, 14, and 28 d, biomarkers of aryl hydrocarbon receptor activation (AHR), hepatic microsomal ethoxyresorufin-O-deethylase (EROD) activity, and cytochrome P4501A (CYP1A)-associated staining increased 14- to 26-fold and 6- to 14-fold, respectively, in fish fed 7.82 µg PAH · g fish (-1) · d(-1). Cytochrome P4501A-associated staining increased 2- to 9-fold on days 3, 7, and 28 in fish fed 0.66 µg PAH · g fish(-1) · d(-1). Bile fluorescent aromatic compounds served as a biomarker of exposure and confirmed that PAH exposure was consistent over 50 d. DNA damage in blood cells, protein oxidation, and lipid peroxidation in the kidney were biomarkers of oxidative stress and all increased in fish fed 7.82 µg PAH · g fish(-1) · d(-1). Fish fed 0.66 µg PAH · g fish(-1) · d(-1) had elevated DNA damage in blood cells but increased protein oxidation or lipid peroxidation in the kidney were not observed. Challenge with Aeromonas salmonicida, at lethal concentration (LC) 20, decreased survival in fish previously fed either 0.66 µg PAH · g fish(-1) · d(-1) or 7.82 µg PAH · g fish(-1) · d(-1) relative to fish fed the control diet. In general, biomarkers of both AHR activation and oxidative stress peaked at 3 to 14 d then declined at 28 to 50 d of PAH exposure and an increase in susceptibility to disease was observed at 50 d. These results link PAH exposure to biomarker responses that may be useful as early indicators of population level responses, such as mortality resulting from an increase in disease susceptibility.

Changes in immune functions in bottlenose dolphins in the northern Gulf of Mexico associated with the Deepwater Horizon oil spill

“…It is plausible that a Th1 reduction and tilt towards a Th2 response in BB 2011, if biologically significant despite not being statistically significant, would increase the susceptibility of those dolphins to Brucella infection or other intracellular pathogens. Increased susceptibility to bacterial challenges, including intra-cellular Mycobacterium marinum, upon PAH exposure was specifically confirmed in several studies in fish (Bravo et al 2011, Prosser et al 2011.…”

The Protective Effect of Selenium on Oxidative Stress Induced by Waterpipe (Narghile) Smoke in Lungs and Liver of Mice

“…The smoking from only one waterpipe episode contains 8 times carbon monoxide, 3 times nitric oxide, 4-15 times acrolien, 6-31 times formaldehyde, and 3-245 times polyaromatic hydrocarbons compared to a smoking of a single cigarette [26]. Notably, many of these toxicants are toxic to tissues and cause alteration of oxidative stress [27].…”

Effects of carcinogenic versus non-carcinogenic AHR-active PAHs and their mixtures: Lessons from ecological relevance

“…Moreover, these CYP1A and EROD showed a trend to decrease over time of exposure following a peak at T 14 that, interestingly, was higher in animals exposed to Phe, a less potent AHR agonist than B[b]F. Although the decrease in CYP MFO activity of protein contents with time of exposure has been described to occur in fish exposed to PAHs, isolated or mixed, carcinogenic, potential carcinogenic and noncarcinogenic (e.g. Costa et al, 2009a;Bravo et al, 2011), the underlying mechanism is not yet understood. There is also indication in vitro that the interactions between high molecular weight, carcinogenic PAHs, do modulate the AHR pathway, production of specifics metabolites and, therefore, carcinogenicity (e.g.…”