Effect Threshold for Selenium Toxicity in Juvenile Splittail, Pogonichthys macrolepidotus A

In fish, selenium can bioaccumulate and cause adverse impacts. One of the fish species potentially at risk from selenium in the San Francisco Bay (California, USA) is the splittail (Pogonichthys macrolepidotus). Previous studies have derived a whole body NOAEL and LOAEL of 9.0 and 12.9 mg/kg-dw, respectively, for selenium in juveniles. However, the NOAEL/LOAEL approach leaves some uncertainty regarding the threshold of toxicity. Therefore, the raw data from the original experiment was re-analyzed using a logistic regression to derive EC10 values of 0.9 mg/kg-dw in feed, 7.9 mg/kg-dw in muscle, 18.6 mg/kg-dw in liver for juvenile splittail. Selenium concentrations in the dietary items of wild splittail exceed the EC10 values derived here. Thus, deformities previously reported in wild splittail may have resulted from selenium exposures via the food chain

Oxidative stress and immunologic responses following a dietary exposure to PAHs in Mya arenaria

<p>Abstract</p> <p>Background</p> <p>The aim of this research was to investigate oxidative stress and immune responses following a dietary polycyclic aromatic hydrocarbon (PAH) exposure in a marine bioindicator organism, the soft shell clam, <it>Mya arenaria</it>. Immune parameters in hemolymph (haemocyte number, efficiency of phagocytosis and haemocyte activity) and assessment of oxidative stress using catalase (CAT) activity and levels of malondialdehyde (MDA) performed on the digestive gland were estimated as biomarkers in clams fed in mesocosm with PAH contaminated phytoplankton. MDA levels and CAT activities were also measured <it>in situ </it>in organisms sampled in a control site (Metis Beach, Québec, Canada) as well as organisms sampled in a site receiving domestic effluents (Pointe-au-Père, Québec, Canada), to assess effects of abiotic variables related to seasonal variations and mixed contamination on the selected parameters.</p> <p>Results</p> <p>Results on immune parameters suggest that the PAHs may interfere with the maturation and/or differentiation processes of haemocytes. MDA results showed that lipid peroxidation did not occur following the exposure. The levels of CAT activity corresponded to weak antioxidant activity (no significant differences). Recovery was noted for all the immune endpoints at the end of the experiment.</p> <p>Conclusion</p> <p>Results suggest that immune parameters are early biomarkers that can efficiently detect a physiological change during a short term exposure to low concentrations of PAHs. The <it>in situ </it>survey (in the natural environment) suggested that clams from the Pointe-au-Père site did not show any oxidative stress as well as the clams contaminated in mesocosm, probably due to the low concentrations of PAHs used for this study. MDA levels increased however in organisms from Metis Beach, a response probably related to domestic effluents or parasitism.</p

Does the early frog catch the worm? Disentangling potential drivers of a parasite age–intensity relationship in tadpoles

The manner in which parasite intensity and aggregation varies with host age can provide insights into parasite dynamics and help identify potential means of controlling infections in humans and wildlife. A significant challenge is to distinguish among competing mechanistic hypotheses for the relationship between age and parasite intensity or aggregation. Because different mechanisms can generate similar relationships, testing among competing hypotheses can be difficult, particularly in wildlife hosts, and often requires a combination of experimental and model fitting approaches. We used field data, experiments, and model fitting to distinguish among ten plausible drivers of a curvilinear age–intensity relationship and increasing aggregation with host age for echinostome trematode infections of green frogs. We found little support for most of these proposed drivers but did find that the parsimonious explanation for the observed age–intensity relationship was seasonal exposure to echinostomes. The parsimonious explanation for the aggregated distribution of parasites in this host population was heterogeneity in exposure. A predictive model incorporating seasonal exposure indicated that tadpoles hatching early or late in the breeding season should have lower trematode burdens at metamorphosis, particularly with simulated warmer climates. Application of this multi-pronged approach (field surveys, lab experiments, and modeling) to additional parasite–host systems could lead to discovery of general patterns in the drivers of parasite age–intensity and age–distribution relationships