Hepatic disorders caused by the intake of ciguatoxins (C-CTX1) in goldfish (Carassius auratus)

Abstract

Ciguatoxins (CTXs) are potent neurotoxins responsible for the ciguatera poisoning (CP). This disease is the most prevalent foodborne illness caused by nonbacterial organisms reported worldwide. Despite this, few research have been conducted to elucidate the CTX metabolism in fish. It has been observed that the ingestion of flesh contaminated with C-CTX1 produced changes in the liver metabolome. These alterations are related to the Glucose-Alanine cycle and increased ammonium ion (NH4+) production. Based on this, a study of biometric indexes and an experiment to determine the possible variations in the ammonia (NH3) excretion in goldfish were performed. After 43 days of CTX-enriched ingestion, it was noted that these animals showed a higher hepatosomatic index (HSI) with respect to those that received nontoxic flesh, while the gonadosomatic index (GSI) was lower in the toxic ones. Two animals, refereed as ‘Detox’, returned to commercial feed for more than 60 days to assess a possible recovery. These animals exhibited the highest HSI (approximately 2 times higher than that in the non-toxic group) and the lowest GSI. Furthermore, the condition factor (CF) and the viscerosomatic index (VSI) was similar in the toxic and nontoxic groups, but the detox showed higher CF and VSI. On the other hand, an increase in NH3 levels was noticed in the aquarium where the fish ingested toxic meat compared to the non-toxic aquarium, reaching a 3-fold higher concentration of this compound. These alterations are in agreement with the hepatic metabolomic alterations observed by nuclear magnetic resonance (NMR) and the Glucose-Alanine cycle.