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https://www.selleckchem.com/products/GDC-0449.html ber of enriched pathways for any tissue or time point (187). Cellular and humoral immune response pathways were considerably impacted in the liver after the recovery period, suggesting that the immune system was attempting to respond to potential damage caused from the chronic oil exposure. Our results demonstrate that liver and gill tissues from southern flounder were differentially altered by Deepwater Horizon oiled sediment exposure and that a 30-day recovery period after exposure substantially shifted gene expression and canonical pathway profiles.Anthropogenic activities have led to the enrichment of cadmium in freshwater systems where it is a contaminant of concern for fisheries and aquaculture as it has no known biological function and is toxic at trace concentrations. Yet, knowledge gaps remain regarding effects of chronic exposure to environmentally relevant concentrations on freshwater fish. Thus, the objectives of the current study were to assess chronic impacts of cadmium on channel catfish (Ictalurus punctatus) including how tissue-specific bioaccumulation patterns relate to functions of those tissues over time. We focused on liver and kidneys, and expression of genes related to cellular stress, glucose metabolism, and steroidogenesis. Catfish were exposed to concentrations of 0.5 (control), 2 (low), and 6 (high) μg L-1 Cd from fertilization to six months. Cadmium exposure negatively impacted channel catfish growth and was linked to bioaccumulation of tissue Cd, which followed a dose-related response, where concentrations in trunk kidney > livrvations of the upregulation of genes necessary for glucose metabolism. Hexokinase (HK), glucose-6-phosphatase (G6P), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were significantly elevated in the high treatment relative to controls at 3 months of exposure. Over the study period, exposure also reduced survival of channel catfish from 3 to 6 months. Reduced

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