Temperature alters antioxidant status and induces cell damage in the Amazonian fish tambaqui

Since Amazonian fish live close to their maximum thermal limits, this makes them vulnerable to the effects of global warming. The aim of this study was to evaluate the oxidative stress and antioxidant enzymatic and biochemical responses of the plasma, liver and muscle of tambaqui (Colossoma macropomum) exposed to a rising gradient of water temperature. One hundred and twenty (N = 120) juvenile tambaqui were exposed to four temperature levels, these being: the environmental temperature of the season (T_env – 25.7–30 °C), 31 °C, 34 °C and 37 °C, following a completely randomized design with three replicates for a period of 60 days. Liver and muscle samples were used to determine the levels of the enzymes superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and lipid peroxidation (LPO). Plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. A histopathological damage assessment (HAI) was performed using liver samples and the results showed an increase in lipid peroxidation in the muscle and liver of animals kept at 37 °C in relation to other temperatures. Enzyme responses were tissue-specific in the liver and muscle. In the liver, the reduction of CAT, SOD and GPx levels of the animals was observed at 37 °C compared to those maintained at T_env and SOD and GPx in relation to animals maintained at 31 and 34 °C. The GPx enzyme showed higher activity at 34 and 37 °C compared to the other evaluated temperatures. At 37 °C, plasma levels of ALT and AST were higher than the other temperatures evaluated, as well as an increase in histopathological damage. In this way, in a scenario of warming of the waters of the Amazon or even of the systems used for rearing of the species, the tambaqui will be able to cope with temperatures of up to 34 °C, without affecting its antioxidant capacity. However, at 37 °C, oxidative stress levels and increased liver damage suggest a reduction in antioxidant capacity due to tissue impairment of the organ and general loss of animal performance as it approaches the upper thermal limit of the species.