Life-time exposure to waterborne copper III: Effects on the energy metabolism of the killifish Poecilia vivipara
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abstract
Copper ions (Cu) are essential to life maintenance, nonetheless, elevated concentrations can be hazardous. Acute and sub-chronic toxic effects of this metal are well known and are usually related to enzymatic inhibition, elevated ROS production and dysfunction of energy metabolism. Despite that, chronic studies are extremely rare. Therefore, the aim of this study was to assess the effects of chronic exposure to 5, 9 and 20 μg/L Cu (28 ad 345 days) on the energy metabolism and survival of the killifish Poecilia vivipara. To accomplish that, we evaluated the activity of enzymes related to aerobic (pyruvate kinase (PK); citrate synthase (CS)) and anaerobic metabolism (lactate dehydrogenase (LDH)) in whole-body (28 days) or in gills, liver and muscle (345 days) of exposed fish. Additionally, whole-body oxygen consumption was evaluated in fish exposed for 28 days and hepatic and muscular expression of genes involved in mitochondrial metabolism (cox I, II and III and atp5a1) was assessed in animals exposed for 345 days. Finally, final survival was evaluated. Following 28 days, Cu did not affect survival neither enzyme activities. However, increased whole-body oxygen consumption was observed in comparison to control condition. After 345 days, 76.8%, 63.9%, 60.9% and 0% survival were observed for control, 5, 9 and 20 μg/L groups, respectively. Animals exposed to 5 and 9 μg/L had a significant reduction in branchial and muscular LDH activity and in hepatic PK activity. Also, exposure to 9 μg/L significantly increased hepatic CS activity. For gene expression, Cu down-regulated muscular cox II (9 μg/L) and III (5 and 9 μg/L), and up-regulated hepatic atp5a1 (9 μg/L). Findings reported in the present study indicate that chronic exposure to Cu induces tissue-specific responses in key aspects of the energetic metabolism. In gills and muscle, Cu leads to reduced energy production through inhibition of anaerobic pathways and mitochondrial respiratory chain. This effect is paralleled by an increased ATP consumption in the liver, characterized by the augmented CS activity and atp5a1 expression. Finally, reduced PK activity indicate that oxidative stress may be involved with the observed outcomes.
