40 research outputs found

    Beta-N-methylamino-L-alanine (BMAA) and isomers : distribution in different food web compartments of Thau lagoon, French Mediterranean Sea

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    The neurotoxin BMAA (beta-N-methylamino-L-alanine) and its isomer DAB (2,4-diaminobutyric acid) have been detected in seafood worldwide, including in Thau lagoon (French Mediterranean Sea). A cluster of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease associated with BMAA, has also been observed in this region. Mussels, periphyton (i.e. biofilms attached to mussels) and plankton were sampled between July 2013 and October 2014, and analyzed using HILIC-MS/MS. BMAA, DAB and AEG (N-(2-aminoethyl)glycine) were found in almost all the samples of the lagoon. BMAA and DAB were present at 0.58 and 0.83, 2.6 and 33, 4.0 and 7.2 mu g g(-1) dry weight in plankton collected with nets, periphyton and mussels, respectively. Synechococcus sp., Ostreococcus tauri, Alexandrium catenella and eight species of diatoms were cultured and screened for BMAA and analogs. While Synechococcus sp., O. tauri and A. catenella did not produce BMAA under our culture conditions, four diatoms species contained both BMAA and DAB. Hence, diatoms may be a source of BMAA for mussels. Unlike other toxins produced by microalgae, BMAA and DAB were detected in significant amounts in tissues other than digestive glands in mussels

    Cyanobacteria and cyanotoxins in estuarine water and sediment

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    International audienceWhile transfer of freshwater cyanobacteria to estuaries has been observed worldwide, the associated transfer of cyanotoxins is less often reported, in particular the sediment contribution. During fall 2018, we monitored the co-occurrence of cyanobacteria and microcystin (MC) in both the water column and in surface sediments at five stations along a river continuum, from a freshwater reservoir to the coastal area in Brittany, France. Cyanobacteria dominated the phytoplankton community in the water column with high densities at the freshwater sites. Microcystis cells and intracellular MC transfer to estuarine and marine sites were observed with decreasing concentrations in accordance with flow dilution. Extracellular MC showed the opposite trend and increased from upstream to downstream in accordance with the lysing of the cells at elevated salinities. Surface sediment samples contained high densities of colonial Microcystis in freshwater and with decreasing concentrations along the salinity gradient, similar to cells concentrations in the water column. Intracellular MC was detected in sediment at all sites except at the marine outlet suggesting the survival of intact cells. Extracellular MC concentrations in sediment were up to five times higher than intracellular concentrations suggesting incomplete MC degradation. mcyB genes were present at all sites, while mcyA genes were absent at the marine outlet suggesting the presence of toxic strains along the estuary. The high densities of intact colonies of potentially toxic Microcystis in the estuarine sediment strongly suggest that sediments can act as an inoculum of cyanobacteria and cyanotoxins in estuaries

    Alexandrium catenella increases the susceptibility of Crassostrea gigas to pathogenic vibrios: possible implications in oyster mass mortalities in the Mediterranean Thau lagoon

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    National audienceSince several years an alarming worldwide expansion of Harmful Algae Bloom (HAB) was observed in coastal and / or confined waters. Alexandrium catenella, a paralytic shellfish poisoning (PSP) producer, is now regularly found in Thau lagoon (south of France) at concentrations up to 15x106 cellules. l-1. In the same periods, events of oyster’s mortality are also observed causing huge economic losses. The purpose of this study is to investigate the relationship between these toxic events and mortality phenomenon. For that, we conducted a field work to evaluate the presence of the toxic A. catenella in Thau lagoon during the years 2013 and 2014 in which high mortality of oysters spats were observed in spring. At the same time, we experimentally infected spats with the pathogenic bacterium V. tasmaniensis LGP32 and kept them unfed or previously fed either with the toxic alga A. catenella or with nontoxic algae, Alexandrium tamarense or Tisochrysis lutea. Results showed that the toxic alga was present in the lagoon when spats' mortalities occurred suggesting A. catenella could be involved in these events. Moreover, our laboratory experiment showed that the exposure to A. catenella increases the susceptibility of spats to one of its pathogens, V. tasmaniensis LGP32. Those results both together suggest for the first time that, in the environment, toxic algae could be implicated in oysters’ mortality. Further studies should be conducted to determine the main factors of this alga implicated in weakening oysters and their immune system against their pathogen which lead to these large scale mortalitie

    Tissue distribution and elimination of ciguatoxins in Tridacna maxima (Tridacnidae, Bivalvia) fed Gambierdiscus polynesiensis

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    Ciguatera is a foodborne disease caused by the consumption of seafood contaminated with ciguatoxins (CTXs). Ciguatera-like poisoning events involving giant clams (Tridacna maxima) are reported occasionally from Pacific islands communities. The present study aimed at providing insights into CTXs tissue distribution and detoxification rate in giant clams exposed to toxic cells of Gambierdiscus polynesiensis, in the framework of seafood safety assessment. In a first experiment, three groups of tissue (viscera, flesh and mantle) were dissected from exposed individuals, and analyzed for their toxicity using the neuroblastoma cell-based assay (CBA-N2a) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) analyses. The viscera, flesh, and mantle were shown to retain 65%, 25%, and 10% of the total toxin burden, respectively. All tissues reached levels above the safety limit recommended for human consumption, suggesting that evisceration alone, a practice widely used among local populations, is not enough to ensure seafood safety. In a second experiment, the toxin content in contaminated giant clams was followed at different time points (0, 2, 4, and 6 days post-exposure). Observations suggest that no toxin elimination is visible in T. maxima throughout 6 days of detoxification
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