The practice of replacing costly animal-derived proteins with more economical plant proteins has augmented the risk of mycotoxin contamination in fish feeds, including contamination with ochratoxin A (OTA). OTA is a secondary metabolite produced by molds commonly found in fish feeds that causes impairment of performance in several fish species and some hepatic biochemical alterations. However, the pathways involved in hepatic damage remain unknown and are limited to histopathological alterations. Purinergic signaling is a homeostatic system that continuously monitors the internal environment to detect injury primarily by two intercellular messengers: adenosine triphosphate (ATP) and adenosine (Ado). The objective of this study was to determine whether OTA-contaminated feed induces the release of nucleotides in the extracellular milieu, as well as whether ectoenzymes modulate ATP pro-inflammatory effects in liver of tambaqui (Colossoma macropomum). Final mean weight, weight gain (WG), and liver weight were significantly lower in tambaqui fed feeds containing 1.6 and 2.4 mg OTA/kg feed than in the control group. Liver ATP and Ado levels were significantly higher in tambaqui fed feeds containing 1.6 and 2.4 mg OTA/kg feed compared with control, while no significant difference was observed regarding adenosine diphosphate and adenosine monophosphate levels. Hepatic triphosphate diphosphohydrolase (NTPDase) activity (for ATP) was significantly greater in tambaqui fed feeds containing 1.6 and 2.4 mg OTA/kg feed compared with control, while adenosine deaminase (ADA) activity was lower. No significant difference was observed with respect to hepatic NTPDase activity (for ADP) or for 5′-nucleotidase activity. Finally, levels of liver metabolites of nitric oxide were significantly higher in tambaqui fed feeds containing 1.6 and 2.4 mg OTA/kg feed than in the control group. Based on these data, exposure to 1.6 and 2.4 mg OTA/kg feed impaired tambaqui growth performance associated with final mean weight and WG. Levels of two important intercellular messengers, ATP and Ado, increased in the extracellular space as a consequence of hepatic damage, exerting opposite immune responses. Finally, liver NTPDase and ADA activities were altered to modulate ATP and Ado levels, respectively, exerting anti-inflammatory effects to counteract OTA-induced hepatic injury.

用更经济的植物蛋白替代昂贵的动物源蛋白的做法增加了鱼饲料中霉菌毒素污染的风险，包括och曲毒素A（OTA）污染。OTA是鱼类饲料中常见的霉菌产生的次生代谢产物，会导致几种鱼类的性能下降和某些肝脏生化改变。然而，涉及肝损害的途径仍是未知的，并且限于组织病理学改变。嘌呤能信号传导是一个体内平衡系统，它连续监测内部环境，主要通过两个细胞间信使：三磷酸腺苷（ATP）和腺苷（Ado）来检测损伤。这项研究的目的是确定受OTA污染的饲料是否诱导细胞外环境中核苷酸的释放，巨大巨像）。坦巴基饲喂的每公斤饲料中含有1.6和2.4毫克OTA / kg的饲料的最终平均体重，体重增加（WG）和肝脏重量均显着低于对照组。与对照组相比，坦巴基饲喂的OTA / kg含量为1.6和2.4 mg的饲料中肝脏ATP和Ado的含量明显高于对照组，而腺苷二磷酸和腺苷一磷酸的含量则无明显差异。坦巴基饲喂的含有1.6和2.4 mg OTA / kg饲料的肝三磷酸二磷酸水解酶（NTPDase）活性（相对于ATP）明显高于对照组，而腺苷脱氨酶（ADA）活性则较低。在肝NTPDase活性（对于ADP）或5'-核苷酸酶活性方面没有观察到显着差异。最后，含1.6和2.4 mg OTA / kg饲料的tambaqui饲料中一氧化氮的肝脏代谢产物水平显着高于对照组。根据这些数据，以1.6和2.4 mg OTA / kg饲料暴露会损害tambaqui的生长性能，而最终平均体重和WG则与之相关。肝损伤的结果是细胞外空间中两个重要的细胞间信使ATP和Ado的水平增加，产生相反的免疫反应。最后，改变肝脏NTPDase和ADA的活性以分别调节ATP和Ado的水平，发挥消炎作用以抵消OTA诱导的肝损伤。肝损伤的结果是细胞外空间中两个重要的细胞间信使ATP和Ado的水平增加，从而产生相反的免疫反应。最后，改变肝脏NTPDase和ADA的活性以分别调节ATP和Ado的水平，发挥消炎作用以抵消OTA诱导的肝损伤。肝损伤的结果是细胞外空间中两个重要的细胞间信使ATP和Ado的水平增加，产生相反的免疫反应。最后，改变肝脏NTPDase和ADA的活性以分别调节ATP和Ado的水平，发挥消炎作用以抵消OTA诱导的肝损伤。