Impact of high temperature, CO2 and parasitic infection on inflammation, immunodepression and programmed cell death in Colossoma macropomum at the transcriptional level.

The production of tambaqui Colossoma macropomum has recently reached a milestone, being considered the main native species produced in South American continental waters. Despite the importance of this fish, its immunity is poorly understood, and global warming could pose severe risks to its health as increasing water temperature leads to an increase in the incidence of parasitic diseases. In an experimental context based on the high-emission scenario of the 5th Intergovernmental Panel on Climate Change (IPCC) report, we evaluated the synergistic effect of exposure to the extreme climate change scenario (RCP8.5) during two exposure periods (7 and 30 days) and two levels of parasitism by monogeneans (low and high). The goal was to understand how the tambaqui immune system will react to this challenge. To achieve this goal, we analyzed the expression of nine immunity-related genes (jak3, stat3, il-10, socs1, casp1, il-1ß, tp53, bcl2, and hif-1α) in the spleen. Our main findings showed downregulation in the jak3/stat3 pathway, genes related to the control of inflammation and apoptosis, in addition to upregulation of proinflammatory genes and those related to pyroptosis during the first 7 days of exposure to the extreme climate scenario, also indicating a stage of immunodepression in these animals. After 30 days of exposure, all genes tended to return to similar levels in the current scenario, possibly due to the decrease in parasite load caused by chronic exposure to the extreme scenario. Our data strongly suggest that the increase in parasitism intensity caused by the extreme climate change scenario is responsible for disturbances in the host's immune system. However, more studies are needed to clarify this poorly understood cascade of events.

Temporal exposure to malathion: Biochemical changes in the Amazonian fish tambaqui, Colossoma macropomum.

The main toxicity mechanism of organophosphate insecticides such as malathion is the acetylcholinesterase enzyme inhibition. However, fish responses to organophosphates may vary depending on the activation of different defense mechanisms as well as the length of exposure. As such, the evaluation of acetylcholinesterase activity, in combination with the evaluation of biotransformation and antioxidants enzymes levels, is useful for indicating damage in fish exposed to this insecticide. Moreover, evaluating mitochondrial activity might evidence how the hierarchic responses occur in relation to the length of time that the fish is exposed. Therefore, the aim of our study is to evaluate whether the length of exposure to malathion differentially affects the biochemical responses of tambaqui. Our hypothesis is that the physiological alterations due to exposure are time dependent. Fish were exposed to sublethal concentrations of the insecticide during 6, 12, 24, 36, and 48 h. Contrary to expectations, there was no acetylcholinesterase activity inhibition during the experiment, which indicates an absence of neurotoxicity. Phase II biotransformation mechanism was activated early, especially in the liver. Oxidative damage was evident in the first hours of exposure and was concurrent with the activation of antioxidant enzymes. Mitochondrial bioenergetics were differentially affected by the length of exposure. The data suggest that the tambaqui regulates mitochondrial respiration differently over time, seeking to maintain homeostasis and ATP demand, and ensures the activation of response mechanisms, thus minimizing oxidative damage and avoiding the neurotoxicity of malathion.

Ecophysiology, genotoxicity, histopathology, and gene responses of naphthalene injected Colossoma macropomum (Cuvier, 1818) exposed to hypoxia.

The present study aimed to evaluate the biological responses of Colossoma macropomum to naphthalene injection and subsequent hypoxia exposure, emphasizing the expression of the tumor suppressor gene tp53. Tambaquis were intraperitoneally injected with naphthalene (50 mg/kg) and, after 96 hours, the fish were transferred to respirometry chambers and, submitted to progressive hypoxia for the determination of critical PO2. In a subsequent experiment, the fish received an intraperitoneal injection of naphthalene and were kept for 96 hours under normoxia. Successively, fish were challenged with acute hypoxia (PO2