We have previously demonstrated in a companion work that acclimation to 28 °C potentiated waterborne copper (Cu) toxic effects in Poecilia vivipara through oxidative stress-related processes. In the present study, we hypothesized that these results were related to kinetic metabolic adjustments in enzymes from aerobic and anaerobic pathways. To test this, P. vivipara was acclimated to two temperatures (22 °C or 28 °C) for three weeks and then exposed to Cu (control, 9 or 20 μg/L) for 96 h. The activity of enzymes from glycolysis (pyruvate kinase [PK] and lactate dehydrogenase [LDH]), Krebs cycle (citrate synthase [CS]) and the electron transport chain system (ETS) were assessed in gills, liver and muscle. Interactive effects were only seen for hepatic LDH activity, as both metal exposure and heat stress, combined or not, inhibited this enzyme, showing a suppression in anaerobic pathways. Conversely, a Cu main effect was present in the liver, expressed as an elevation in ETS activity, showing an enhancement in hepatic aerobic metabolism likely related with the very energy-demanding process of metal detoxification. Moreover, this study shows that P. vivipara has a remarkable ability to compensate heat stress in terms of energy metabolism, as we could not observe acclimation temperature effects for most of the cases. Nonetheless, a tissue-dependent effect of elevated temperature was observed, as we could observe an inhibition in muscular CS activity. Finally, it is concluded that kinetic adjustments in terms of the energy metabolism are not related with the temperature-dependent elevation of Cu toxicity in P. vivipara as we previously hypothesized.
Keywords: Biomarker; Ecotoxicology; Energy metabolism; Enzymatic activity; Heat stress; Trace metals.
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