Chronic exposure to environmental cadmium affects growth and survival, cellular stress, and glucose metabolism in juvenile channel catfish (Ictalurus punctatus).

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 > liver = head kidney >> muscle. Differences in tissue Ca, Cu, Fe, and Zn concentrations were also observed between treatments. Following 3 months of exposure, expression of metallothionein (MT) and heat shock proteins (HSP) 70 & 90 increased relative to controls; however, no differences were detected at 6 months, suggesting compensation. Conversely, there were no differences in expression patterns for key genes in steroidogenesis, steroidogenic factor 1 (SF1), steroidogenic acute regulatory protein (StAR), and cytochrome P450scc (P450), which supports the observation that Cd did not affect the secondary stress response, evaluated via plasma cortisol and glucose concentrations following a low water stress event. As a function of length and weight, the high Cd treatment yielded fish that were significantly smaller than controls. In addition to the cellular responses in MT and HSPs noted, reduced growth in the high Cd treatment was likely due, at least in part, to elevated energetic demands. This is supported by observations 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 fitness, as a consequence of cadmium exposure, could be visible at the population level through altered life histories and growth patterns.