Abstract

Early life-stages of the endangered white sturgeon (Acipenser transmontanus) have been shown to be among the most sensitive fishes to aqueous copper (Cu) exposure. In a recent analogous study, we examined the role of whole-body Cu accumulation and Na homeostasis in species-specific differences between the sensitivity of white sturgeon and a common laboratory fish model, rainbow trout, to Cu. However, the potential roles of important mechanisms such as Cu-induced oxidative stress and/or metallothionein (MT) induction as potential drivers of sensitivity of white sturgeon to Cu have not been investigated to date. Here, rainbow trout and white sturgeon from three different early life-stages were exposed to waterborne Cu for 96 h, following which major antioxidant parameters, lipid peroxidation and MT gene expression were evaluated. Results indicated that during larval and swim-up life-stages, Cu induced oxidative damage in white sturgeon was greater than in rainbow trout. Moreover, baseline glutathione (GSH) was significantly greater in rainbow trout than white sturgeon. Observations also suggested that trout exceedingly relied on GSH to combat Cu-induced oxidative stress as they grew older. In contrast, sturgeon recruited an increasing level of MT to neutralize Cu-induced oxidative stress and/or Cu loading. In our recent study, we demonstrated that Na homeostasis is more susceptible to Cu in white sturgeon than in rainbow trout. Collectively, these findings indicate that the greater degree of oxidative damage in early life-stages, in addition to the higher magnitude of the disruption of Na homeostasis, contributes to the higher sensitivity of white sturgeon to Cu exposure.

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