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In this study, we measured the interactive effect of temperature (22 degrees C and 28 degrees C) and waterborne copper (Cu) contamination (9 mu g/L and 20 mu g/L) on the killifish Poecilia vivipara. Endpoints analyzed included parameters involved in Cu-accumulation, antioxidant capacity (antioxidant capacity against peroxyl radicals [ACAP] and total antioxidant capacity [TAC]), oxidative damage (lipid peroxidation [LPO]) and upper thermal tolerance (critical thermal maximum [CTMax]). Results show that Cu hepatic accumulation was elevated in 28 degrees C in comparison to 22 degrees C in both exposure groups. For gills, this was true only in 20 mu g/L. Moreover, hepatic and brachial accumulation were concentration-dependent in both acclimation temperatures. Additionally, Hepatic ACAP and TAC were elevated in animals acclimated to 28 degrees C and only the animals kept at this temperature had reduced ACAP and TAC levels facing metal exposure (9 and 20 mu g/L). Similarly, the combination of elevated temperature and Cu exposure raised hepatic LPO levels. Finally, animals acclimated to 28 degrees C had higher CTMax levels in comparison to fish acclimated to 22 degrees C both in control and exposed animals, however, CTMax of contaminated fish were only reduced in comparison to control in animals kept at 28 degrees C. Concluding, we show that the physiological mechanism besides the potentiating effect of elevated temperature in Cu toxicity is related to higher hepatic and branchial metal accumulation and elevated oxidative stress in the liver, outlined by reduced antioxidant capacity and elevated oxidative damage. We also show that these outcomes lead to compromised organismal performance, characterized by reduced CTMax. Finally, it is concluded that Cu exposure in warmer periods of the year or within global warming predictions may be more hazardous to fish populations.