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The aim of this study was to verify the carryover of aflatoxin B from feed to lambari fish. Aflatoxins (AF) were incorporated into feed, checking the levels by HPLC. Treatments were: Control, feed without toxin; A, feed + 10 µg AFB kg; B, feed + 20 µg AFB kg; and C, feed + 50 µg AFB kg. Juveniles of lambari fish were placed in 12 aquariums at a density of 50 fish/m. Fish were fed twice a day with extruded feed, at 5% of animal biomass. The unit sample was constituted by a pool of 10 fish. AFs B, B, G, G and M were quantified by HPLC in fish muscle and liver after 30, 60, 90 and 120 days of experiment. There was accumulation of AFs is fish liver and muscle, mainly after 90 days. Fish from treatment C had higher levels of AFB in muscle when compared with the others, and AFB in muscle at 120 days was similar to the levels in feed. Therefore, when lambari fish is exposed on a daily and long-term basis to AFs in feed, the regulation limits for AFs in animal feed do not guarantee safety for consumers.

Aflatoxins (AF) can be cumulative in fish tissues and can influence weight, length, feed intake and survival depending on the species. The aim of this work is to measure performance and aflatoxin levels in tissues of matrinxã (Brycon cephalus) fish chronically exposed to aflatoxin. Aflatoxin was incorporated into fish diets at the following levels: Control Feed + 0 μg AFB1 kg-1; A. Feed + 10 μg AFB1 kg-1; B. Feed + 20 μg AFB1 kg-1; C. Feed + 50 μg AFB1 kg-1. It was used one tank per treatment, each one with 150 juvenile fish, and three replicates within each tank were used for sampling, that was carried out monthly over a period of six months. Aflatoxin was quantified by HPLC in fish liver and muscle after clean up using immunoaffinity columns. Performance was evaluated by using weight, length, consumption and survival rate. Muscle and liver aflatoxin levels were below the limit of detection in all control samples. Aflatoxins B2, G1 and G2 were not detected in any tissues. Traces (values between limits of detection and quantification) of AFB1 were observed in liver tissue in treatment A from day 30 through 90, reaching 0.32 μg AFB1 kg-1 at 150 days of exposure. Treatment B presented traces up to day 60 and had, with a maximum level of 0.39 μg AFB1 kg-1 at 150 days of exposure. Treatment C had aflatoxin residues after day 30, with values ranging from 0.17 to 0.61 μg AFB1 kg-1 during exposure. Muscle samples only had traces of AFB1 in all treatments. Fish was affected by exposure to AFB1 with higher values (P<0.05) for weight and length in treatments A, B and C relative to controls. Therefore, results indicate that matrinxã do not accumulate AFB1 residues in edible tissues, but chronic exposure affects the species.

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The objective of this work was to evaluate the aflatoxins residues on tissues of Pacu (Piaractus mesopotamicus) fish chronically exposed to dietary aflatoxins, also evaluating the effects on fish performance. Aflatoxins were incorporated into the extruded fish feed and the concentrations were confirmed by high performance liquid chromatography (HPLC). The experimental design comprised the following treatments: Control – feed without toxin; Treatment A: feed + 10 μg aflatoxin B1 (AFB1)/kg; Treatment B: feed + 20 μg AFB1/kg and Treatment C: feed + 50 μg AFB1/kg. Pacu juvenile were allocated in tanks with density of one fish per litter. The experiment lasted 180 days with monthly sampling, and approximately ten fish per treatment were used to compose a sample. Biometric surveys were performed every 30 days, including standard weight and length. Aflatoxins were detected and quantified in fish muscle and liver by HPLC, using immunoafinity columns. Results showed AFB1 deposition in the liver throughout the experiment in all treatments, but only treatment C differed significantly (P<0.05) from the others after 150 days, while in muscle there was low residual deposition. Long-term exposed fish had negative influence in weight and length. The higher mortality was observed in treatment C. Although there were AFB1 residues at low levels in liver and only a slight amount in fish muscle, it should be noted that accumulation is possible in the Pacu species. The diets contaminated with AFB1 negatively interfered in weight and length of fish when compared to control. Therefore, it can be concluded that long-term exposure of Pacu to dietary AFB1 can cause losses to producers.

The objective of this study was to evaluate biochemical parameters and histopathology of liver in Matrinxã (Brycon cephalus) and Pacu (Piaractus mesopotamicus) fish chronically exposed to dietary aflatoxins. Fish feed was artificially contaminated with aflatoxins and the treatments were: Control – feed without toxin; Treatment A – feed + 10 μg aflatoxin B1 (AFB1)/kg; Treatment B – feed + 20 μg AFB1/kg; and Treatment C – feed + 50 μg AFB1/kg. Matrinxã and Pacu juvenile fish were placed in tanks for 180 days. Five experimental units per treatment were monthly sampled and submitted to blood collection and removal of hepatic tissue. Thus, twenty blood and liver samples for each species were collected monthly, adding up to 240 samples analysed. To verify biochemical changes, analyses included total proteins, albumin, globulins, aspartate aminotransferase (AST) and alkaline phosphatase (ALP). The hepatic tissue was examined microscopically and the slides presenting histopathological changes were photo-documented. There was effect of treatment (P<0.05) for AST and ALP in Matrinxã, while no effect (P>0.05) was observed in Pacu. A reduction (P<0.05) in AST and ALP values during the time of exposure was observed in all treatments for both species. Fatty degeneration and liver damage were observed for both species in treatments exposed to aflatoxins. Fatty degeneration in Pacu was noticed after 30 days of exposure, while in Matrinxã it was observed after 60 days. Disorganisation of the hepatocyte cord arrangement was also observed in those treatments exposed to aflatoxin, following 90 days of exposure in Matrinxã, and after 60 days in Pacu. Therefore, aflatoxins have little influence on biochemical parameters in the species evaluated. However, exposure to aflatoxins caused liver changes, such as cell death, fatty and hydropic degeneration, thus it could be concluded that both species are susceptible to the toxic effects of long-term exposure to dietary AFB1.

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The aim of this study was to detect and quantify fumonisin B1 (FB1) in cereal mixtures marketed in Brazil. Fifteen samples from different lots were acquired each month by internet from supermarkets during seven months, adding up to 105 analysed samples. The unit sample constituted of an original package with a minimum of 250 g. Extraction and clean-up of samples for FB1 determination were carried out using immunoaffinity columns. Identification and quantification of FB1 were performed by high performance liquid chromatography. Eighty-eight (83.8%) samples were contaminated with FB1 and four (3.8%) presented levels above 500 µg kg(-1) (634, 703, 1269 and 1876 µg kg(-1)). Maximum FB1 + FB2 levels allowed by Brazilian regulations will reach 1500 µg kg(-1) for corn flour in 2016 and 1000 µg kg(-1) for others corn products. This study showed that even at levels below the legislative limits, human exposure to this toxin can occur constantly.