Metabolic Hepatic Disorders Caused by Ciguatoxins in Goldfish (Carassius auratus)

Simple Summary: Ciguatoxins (CTXs) are potent neurological marine toxins able to cause ciguatera poisoning (CP) in humans via the food web. Although considered one of the most important foodborne diseases in the world, little is known about how CTXs are metabolized in fish, and the possible alteration of hepatic metabolomic linked to these toxins. To clarify this aspect, goldfish (Carassius auratus) were fed with C-CTX1 enriched flesh, and their livers were analyzed by nuclear magnetic resonance (NMR). Altered concentrations of glucose, glycogen, taurine, alanine, and lactate were observed. Furthermore, an increase in liver size was noted in animals fed a toxic diet. In addition, increased ammonia concentrations in the aquarium with toxic feed were detected. These results suggest that C-CTX1 ingestion leads to changes in liver metabolomic, which are related to the glucose-alanine cycle. This is the first evidence of CTXs-mediated alterations in liver metabolomic, and a step to further elucidate the metabolism of these toxins within fish. Ciguatera poisoning (CP) is a foodborne disease known for centuries; however, little research has been conducted on the effects of ciguatoxins (CTXs) on fish metabolism. The main objective of this study was to assess different hepatic compounds observed in goldfish (Carassius auratus) fed C-CTX1 using nuclear magnetic resonance (NMR)-based metabolomics. Thirteen goldfish were treated with C-CTX1-enriched flesh and sampled on days 1, 8, 15, 29, 36, and 43. On day 43, two individuals, referred to as 'Detox', were isolated until days 102 and 121 to evaluate the possible recovery after returning to a commercial feed. At each sampling, hepatic tissue was weighed to calculate the hepatosomatic index (HSI) and analyzed for the metabolomics study; animals fed toxic flesh showed a higher HSI, even greater in the 'Detox' individuals. Furthermore, altered concentrations of alanine, lactate, taurine, glucose, and glycogen were observed in animals with the toxic diet. These disturbances could be related to an increase in ammonium ion (NH4+) production. An increase in ammonia (NH3) concentration in water was observed in the aquarium where the fish ingested toxic meat compared to the non-toxic aquarium. All these changes may be rationalized by the relationship between CTXs and the glucose-alanine cycle.