Dietary exposure to ochratoxin A reduces growth performance and impairs hepatic purinergic signaling in tambaqui (Colossoma macropomum).

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.

Dietary ochratoxin A (OTA) decreases growth performance and impairs muscle antioxidant system and meat fatty acid profiles in juvenile tambaqui (Colossoma macropomum).

Plant-based ingredients are successfully replacing fishmeal in fish feeds. However, this practice increases the risk of feed contamination by mycotoxins that reduce production and heath associated with oxidative damage. The aim of this study was to determine whether feed contaminated with environmentally relevant concentrations of ochratoxin A (OTA) causes muscle oxidative damage in tambaqui (Colossoma macropomum), and to determine whether this feed impairs fatty acid profiles in fish meat. Final mean weight, weight gain, daily weight gain, feed efficiency, and specific growth rate were significantly lower in fish fed 1.6 and 2.4 mg OTA/kg compared to those fed basal diet, while feed conversion was significantly higher in these same groups compared to the basal group. Levels of reactive oxygen species and lipid peroxidation in muscle were significantly higher in fish fed 1.6 and 2.4 mg OTA/kg compared to those in the basal group. Likewise, muscle superoxide dismutase and glutathione peroxidase activities were significantly higher in fish fed 1.6 and 2.4 mg OTA/kg then in those fed basal feed. The total content of saturated fatty acids was significantly higher, and total content of polyunsaturated fatty acids was significantly lower in fish fed 2.4 mg OTA/kg compared to those fed basal feed. Taken together, the data suggest that OTA-contaminated feed induces oxidative damage and disturbs enzymatic and non-enzymatic antioxidant responses in tambaqui meat. The perturbations of fatty acid profiles in fish meat appears to mediated by oxidative damage, representing negative impact on fish health and presenting concerns for consumers of fish.