Cadmium accumulation and interactions with zinc, copper, and manganese, analysed by ICP-MS in a long-term Caco-2 TC7 cell model

The influence of long-term exposure to cadmium (Cd) on essential minerals was investigated using a Caco-2 TC7 cells and a multi-analytical tool: microwave digestion and inductively coupled plasma mass spectrometry. Intracellular levels, effects on cadmium accumulation, distribution, and reference concentration ranges of the following elements were determined: Na, Mg, Ca, Cr, Fe, Mn, Co, Ni, Cu, Zn, Mo, and Cd. Results showed that Caco-2 TC7 cells incubated long-term with cadmium concentrations ranging from 0 to 10 lmol Cd/l for 5 weeks exhibited a significant increase in cadmium accumulation. Furthermore, this accumulation was more marked in cells exposed long-term to cadmium compared with controls, and that this exposure resulted in a significant accumulation of copper and zinc but not of the other elements measured. Interactions of Cd with three elements: zinc, copper, and manganese were particularly studied. Exposed to 30 lmol/l of the element, manganese showed the highest inhibition and copper the lowest on cadmium intracellular accumulation but Zn, Cu, and Mn behave differently in terms of their mutual competition with Cd. Indeed, increasing cadmium in the culture medium resulted in a gradual and significant increase in the accumulation of zinc. There was a significant decrease in manganese from 5 lmol Cd/l exposure, and no variation was observed with copper. Abbreviation: AAS – Atomic absorption spectrometry; CRM– Certified reference material; PBS – Phosphate buffered saline without calcium and magnesium; DMEM – Dubelcco’s modified Eagle’s medium

Paralytic phycotoxin uptake by scallops (Pecten maximus)

It is difficult to apply sanitary standards for mollusc contamination by paralytic shellfish poisoning to animals not consumed whole. This problem is illustrated by the 1990 embargo on a Japanese shipment of frozen scallop muscle and gonad: the sanitary threshold applied to digestive gland (in Japan) does not guarantee that muscle and especially gonad are toxin-free. Accordingly, we performed experimental contaminations of scallops (Pecten maximus) from Port-en-Bessin (Normandy, France) using a toxic Japanese strain of Alexandrium tamarense. During the contamination/decontamination experiment on different tissues (digestive gland, muscle, gonad), extracts were obtained using cold acetic acid 0.1 N to maintain the perfect integrity of the toxin profile. These initial trials indicated that with a daily concentration of 2 × 106 cells. 1-1 a maximum toxicity equivalent to 850 μg.100 g-1 of digestive gland meat was attained in 2 weeks. Concerning toxin profiles, it would appear that gonad can selectively accumulate gonyautoxins, particularly GTX2/GTX3, even though the relative amount of uptake always follows the order hepatopancreas > gonad > muscle. Morcover, studies of Japanese scallops imported in 1990 showed that 80% of the gonad and muscle samples included all or part of the kidneys and excretory organs, whose relationship with gonad toxicity need further clarification. Finally, the toxin profile of the different organs during decontamination revealed an inversion of the relative proportions of GTX2/GTX3 epimers, as noted by other authors. Confirmation of selective biological conversion between organs will require further study.Les normes sanitaires appliquées à la contamination des bivalves par le poison paralysant des coquillages (PSP) sont difficilement applicables aux coquillages non consommés entiers. C'est le cas des coquilles Saint-Jacques, et l'embargo appliqué en 1990 sur les "containers" japonais contenant des noix et corails congelés, en est un exemple: le seuil sanitaire appliqué à la glande digestive (au Japon) ne garantit pas pour autant que le muscle, et surtout la gonade, soient indemnes de toxines. Pour cette raison nous avons pratiqué des contaminations expérimentales de coquilles (Pecten maximus) provenant de Port-en-Bessin (Normandie) par une souche japonaise toxique d'Alexandrium tamarense. Lors de l'expérience de bioaccumulation/épuration sur différents tissus (glande digestive, muscle, gonade) les extraits ont été réalisés par l'acide acétique 0,l N à froid, ceci afin de garder une intégrité parfaite au profil toxinique. D'après ces premiers essais, il apparaît qu'avec une concentration journalière de 2.106 cellules.1-1 un maximum de toxicité équivalent à 850 μg.100 g-1 de chair de glande digestive est atteint en 15 jours. En ce qui concerne les profils toxiniques, il apparaît, d'une part, que la gonade peut accumuler sélectivement des gonyautoxines, en particulier GTX2 et GTX3, même si l'importance de la bioaccumulation suit toujours l'ordre : hépatopancréas > gonade > muscle. D'autre part, les observations réalisées sur les coquilles japonaises importées en 1990 montrent que 80 % des échantillons gonades et muscles comportaient également les reins ou une partie des reins, organes d'élimination dont la relation avec la toxicité des gonades sera à vérifier. Enfin, le profil toxinique des différents organes en décontamination révèle une inversion des proportions relatives des épimères GTX2/GTX3, comme cela a été observé par d'autres auteurs. Une bioconversion sélective entre organes serait à confirmer ultérieurement

Pinnatoxins’ Deleterious Effects on Cholinergic Networks: From Experimental Models to Human Health

International audiencePinnatoxins (PnTXs) are emerging neurotoxins that were discovered about 30 years ago. They are solely produced by the marine dinoflagellate Vulcanodinium rugosum, and may be transferred into the food chain, as they have been found in various marine invertebrates, including bivalves. No human intoxication has been reported to date although acute toxicity was induced by PnTxs in rodents. LD 50 values have been estimated for the different PnTXs through the oral route. At sublethal doses, all symptoms are reversible, and no neurological sequelae are visible. These symptoms are consistent with impairment of central and peripheral cholinergic network functions. In fact, PnTXs are high-affinity competitive antagonists of nicotinic acetylcholine receptors (nAChRs). Moreover, their lethal effects are consistent with the inhibition of muscle nAChRs, inducing respiratory distress and paralysis. Human intoxication by ingestion of PnTXs could result in various symptoms observed in episodes of poisoning with natural nAChR antagonists. This review updates the available data on PnTX toxicity with a focus on their mode of action on cholinergic networks and suggests the effects that could be extrapolated on human physiology