PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Shellfish”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources

Assessment of Potential Cancer Risk from Consumption of PCBs Bioaccumulated in Fish and Shellfish.

We evaluated the potential cancer risk to adults from ingesting polychlorinated biphenyls (PCBs) in fish and shellfish using an equilibrium partitioning model of PCB bioaccumulation in the aquatic animal. Estimated potential cancer risk to humans increased exponentially with increasing hydrophobicity of the PCB. However, the addition of food-chain sources of PCBs was necessary to cause potential cancer risk to exceed 10(-6). Environmental degradation of the PCB reduced cancer risk by reducing the exposure concentration; 3.3 degradation half-lives were required to reduce cancer risk estimates by one order of magnitude. PCB biotransformation to nongenotoxic metabolites (no increase in the cancer slope factor) by the aquatic animal reduced cancer risk by reducing the steady-state concentration of PCBs in the edible tissue. Even relatively slow biotransformation (e.g., metabolic half-life of 100 days) reduced cancer risk estimates under the default model conditions. Nonequilibrium conditions, such as limited exposure time, reduced potential cancer risk by reducing contaminant concentrations in the aquatic animal. Risk assessment using toxic equivalency factors predicted substantially greater potential risk for specific congeners than for PCB mixtures. Our evaluation demonstrates that deviation from conventional assumptions used in risk assessment (e.g., negligible biotransformation and degradation; steady-state equilibrium) can significantly affect cancer risk estimates.

Journal Article↗

Uptake and depuration of paralytic shellfish toxins in the green-lipped mussel, Perna viridis: a dynamic model.

Uptake and depuration of paralytic shellfish toxins in the green-lipped mussel, Perna viridis, were investigated by exposing the mussels to dinoflagellates (Alexandrium tamarense, ACTI01) under laboratory conditions for 8 d, then depurating them in clean seawater for 14 d. First-order linear differential equations were set up for five tissue compartments: Viscera, gill, hepatopancreas, adductor muscle, and foot. The solutions to these equations were used to fit the experimental data. We then estimated the parameters governing the model, which depend on the elimination rate from each compartment and the transfer coefficient between compartments. An assumption of the model is that the gills transport the dinoflagellates directly to the mouth and then to the viscera, where the ingested cells are broken down, releasing the toxins. The toxins absorbed are transferred to other tissues. During the uptake phase, the transfer coefficients from viscera to gill, hepatopancreas, adductor muscle, and foot were 0.03, 0.24, 0.01, and 0.004 per day, respectively. During the depuration phase, the transfer coefficients were 0.01, 0, 0.01, and 0.003 per day, respectively. In terms of the anatomical distribution of N-sulfocarbamoyl-11-hydroxysulfate (C2) toxins in various tissues, viscera and hepatopancreas contained the highest percentages (47-74% and 8-41%, respectively). Together, these two tissue compartments accounted for 71 to 96% of all C2 toxins present. The biokinetic model allows a quantitative prediction of C2 toxins in whole ussel as well as individual tissue compartments based on the density estimates and toxin load of dinoflagellate cells in the surrounding waters over time.

Animals↗

Pathogenic bacteria isolated from disease outbreaks in shellfish hatcheries. First description of Vibrio neptunius as an oyster pathogen.

Shellfish hatcheries are often affected by disease outbreaks. Three such episodes were investigated in different Galician hatcheries in order to establish the relationship between present microbiota and mortalities. Isolates were obtained from various parts of the hatcheries. Experimental tests for pathogenicity were carried out in microscale experiments using selected strains on Ostrea edulis larvae. The pathogenicity of 1 strain from each outbreak was demonstrated and shown to cause high mortalities (ranging from 98.5 to 100%) in 72 to 96 h after inoculation of larval cultures. All 3 strains belong to the genus Vibrio. One of the strains was identified as Vibrio neptunius and is the first description of this species as a molluscan pathogen. The other 2 strains showed low similarity with the Vibrio species analysed and may constitute new species within this genus.

Animals↗

Accumulation of paralytic shellfish poison (PSP) and biotransformation of its components in oysters, Crassostrea gigas, fed with the toxic dinoflagellate Alexandrium tamarense.

As a part of our studies on the mechanism of uptake of paralytic shellfish poison (PSP) and the kinetics of its accumulation in bivalves, oysters Crassostrea gigas were experimentally contaminated with PSP by being fed with the toxic dinoflagellate Alexandrium tamarense for 2, 4, 6, 8 and 10 days. Temporal variations in the PSP contents and their profiles in oysters during the feeding experiment were monitored by high-performance liquid chromatography (HPLC) and the toxin profile of the oysters was compared with that of A. tamarense. Toxins excreted from the infested oysters into the seawater for 2 and 10 days were recovered and analyzed by HPLC. PSP toxicity rapidly appeared in the tissues of oysters and their toxicity levels reached 0.6 (0.3), 2.2 (1.1), 1.0 (0.5), 3.4 (1.6) and 1.1 (0.5) MU/g (nmol/g) shucked meat at 2, 4, 6, 8 and 10 days, respectively. The accumulation rates of toxin, calculated from the total amount (nmol) of toxins expressed by the total cell number fed during the exposure period and the toxicity of the oysters, were 14.1, 18.7, 5.1, 14.9 and 3.2% for 2, 4, 6, 8 and 10 days. During feeding experiments, the toxin profile of oysters changed substantially, showing marked differences from the proportions found in the toxigenic dinoflagellate used as food. The toxin components in this strain existed almost exclusively as beta-epimers, which accounted for 66.3 mol% of the total. This contrasts with the case of the oysters, where the beta-epimers represented 24.8, 29.8, 25.1, 27.3 and 25.2 mol% of the total at 2, 4, 6, 8 and 10 days, respectively. The amount of gonyautoxin-1 (GTX1) accumulated in oysters increased linearly and slowly for 8 days and the maximum content of GTX1 reached 51.3 mol%. The composition of GTX group compounds recovered from the seawater in which the oysters had been reared was a little different from that within the oyster tissues.

Animals↗

[Lipophilic toxin profiles associated with diarrhetic shellfish poisoning in scallops, Patinopecten yessoensis, collected in Hokkaido and comparison of the quantitative results between LC/MS and mouse bioassay].

Lipophilic toxins associated with diarrhetic shellfish poisoning (DSP) in scallops, Patinopecten yessoensis, collected in Hokkaido, Japan were quantified by liquid chromatography-mass spectrometry (LC/MS). Pectenotoxin-6 (PTX6) and yessotoxin (YTX) were the dominant toxins in the scallops, although the percentages of these toxins were different depending on the production area or the sampling period. The quantitative results obtained for the scallops in LC/MS and in mouse bioassay (MBA) were compared. Fifty of the 55 samples found to be exceeding the local quarantine level (0.025 MU/g whole meat) in Hokkaido by LC/MS were quantified by MBA as being below the quarantine level. It is suggested that this discrepancy is due to poor detection of YTX by MBA. These results indicate that LC/MS is a better method than MBA in terms of sensitivity and accuracy to quantify known lipophilic toxins, including YTX.

Animals↗

Canning process that diminishes paralytic shellfish poison in naturally contaminated mussels (Mytilus galloprovincialis).

Changes in toxin profile and total toxicity levels of paralytic shellfish poison (PSP)-containing mussels were monitored during the standard canning process of pickled mussels and mussels in brine using mouse bioassays and high-performance liquid chromatography. Detoxification percentages for canned mussel meat exceeded 50% of initial toxicity. Total toxicity reduction did not fully correspond to toxin destruction, which was due to the loss of PSP to cooking water and packing media of the canned product. Significant differences in detoxification percentages were due to changes in toxin profile during heat treatment in packing media. Toxin conversion phenomena should be determined to validate detoxification procedures in the canning industry.

Animals↗

Paralytic shellfish poisoning toxins accumulation in purple clam Hiatula rostrata and toxic effect on milkfish Chanos chanos larval fish.

In an attempt to feed purple clams (Hiatula rostrata) with dinoglagellate Alexandrium minutum, the maximal accumulation toxicity of paralytic shellfish poisoning (PSP) toxins reached 40.6 MU/g on day 5 of feeding. Subsequently, the toxicity increased no further, although purple clams ingested more toxic algae. Furthermore, when milkfish (Chanos chanos) larvae were treated with toxic, nontoxic A. minutum or PSP toxin-containing extract in the water medium, it was found that the mortality of fish increased with the increasing concentrations of toxic algae. PSP toxin-containing extract did not show any toxic effect on milkfish larvae.

Animals↗

Detection of paralytic shellfish poison by rapid cell bioassay: antagonism of voltage-gated sodium channel active toxins in vitro.

Although cytotoxicity assays provide several advantages over mouse bioassays, sodium channel-blocking marine toxins, such as those associated with paralytic shellfish poison (PSP), require prolonged incubation periods of 24-48 h. This is in marked contrast to in vitro detection of sodium channel-enhancing marine toxins such as ciguatoxins or brevetoxins which can be accomplished in as few as 4-6 h. We developed a modified PSP cell bioassay that is as rapid as in vitro methods for sodium channel-enhancing toxins. The cell bioassay is based on a saxitoxin-dependent antagonism of the rapid in vitro effects of brevetoxin or ciguatoxin. Comparative analysis of naturally incurred PSP residues by both antagonism cell bioassay and the mouse bioassay demonstrated significant correlation. The simplicity, sensitivity, and enhanced kinetics of the new antagonism cell bioassay format provide the basis for development of a practical alternative to conventional mouse testing for PSP.

Animals↗

Liquid chromatographic determination of domoic acid in mussels, using AOAC paralytic shellfish poison extraction procedure: collaborative study.

A liquid chromatographic method using the AOAC paralytic shellfish poison (PSP) extraction procedure for domoic acid, a marine toxin, in mussel tissue was collaboratively studied in 10 laboratories. Domoic acid is extracted by boiling the homogenized tissue for 5 min with 0.1N HCl. The mixture is cooled, diluted to a known volume, and then centrifuged. An aliquot of the supernate is diluted, filtered, and analyzed by reverse-phase liquid chromatography with a mobile phase containing acetonitrile and water adjusted to about pH 2.5. Each collaborator received a prepared standard solution, a practice sample, and 7 randomly numbered unknown samples (1 blank mussel tissue, 1 spiked at 14.1 micrograms domoic acid/g, 1 spiked at 18.9 micrograms/g, and duplicate samples with naturally incurred domoic acid at 75 micrograms/g and at 186 micrograms/g). Five of the laboratories had little or no experience in domoic acid analysis. Ten of 11 laboratories completed the study and submitted results. Two individual values out of a total of 70 were found to be outliers. Mean recovery of domoic acid from the spiked extracts was 75%. Relative standard deviations between laboratories (RSDR) ranged from 7.5 to 19.4%; within-laboratory RSDs (RSDr) for the 2 blind duplicate pairs were 1.9 and 4.8%. The detection limit was about 1 microgram domoic acid/g. The method has been adopted official first action by AOAC.

Animals↗

Anaphylaxis to grand keyhole limpet (abalone-like shellfish) and abalone.

We report five patients who developed moderate to severe anaphylactic reactions induced by the ingestion of grand keyhole limpet (GKL) and abalone. Specific IgE-mediated hypersensitivity to these shellfish was demonstrated by history, prick skin test, and RAST. RAST inhibition technique revealed the cross-antigenicity between GKL, abalone, and keyhole limpet hemocyanin.

Adult↗

Zinc from oyster tissue as causative factor in mouse deaths in official bioassay for paralytic shellfish poison.

Toxicity (extreme weakness, body temperature drop, cyanosis, some slow deaths) in test mice, upon intraperitoneal injection of standard-method paralytic shellfish poison (PSP) extracts of some PSP-free oysters, is consistent with the relatively high levels of zinc in these extracts. As a rough guideline, the threshold for a toxic response corresponds to a drained tissue zinc level of over 900 micrograms/g. The identification of zinc as the substance responsible has been supported by inducing toxicity in control extracts by spiking with nontoxic levels of zinc, and by eliminating toxicity from toxic extracts by chemical removal (precipitation, ion exchange) of metals.

Animals↗

[Clinical analysis of paralytic shellfish poisoning following ingestion of oysters].

We describe five patients of paralytic shellfish poisoning (PSP) following ingestion of oysters in January 1991, in Nagato, Yamaguchi. The five patients (four men and one woman, age range:37-80 years) developed symptoms three-nine hours after consuming oysters. Symptoms included paresthesia of the mouth and tongue (three), paresthesia of the extremities (five), and quadriparesis (five). The median duration of neurological symptoms was 16 hours. All five patients completely recovered. Although PSP is rare as compared with globe fish poisoning in Japan, the fatality rate of PSP is 8%-9%, with deaths occurring in one-12 hours secondary to respiratory failure. PSP is an important disorder for differential diagnosis of acute paralytic illnesses, such as globe fish poisoning, botulism, acute polyradiculoneuropathy, fisher syndrome, myasthenia gravis, and periodic paralysis.

Adult↗

["Paralytic shellfish poisoning" (author's transl)].

In October 1976 an epidemic of 120 cases of paralytic shellfish poisoning was recorded in western Europe. Analysis of the 23 cases seen in Swizterland shows the following data; paresthesia of mouth and lips (100%); cerebellar syndrome (86%) with giddiness, ataxia, dysmetry and floating sensation; paresia or paralysis (62%); digestive symptoms (14%); no death. The mean incubation time is 3 hs 30 min; mean duration of the symptoms is 2 days. Half of the patients complain of asthenia and moderate memory disturbance lasting up to 3 weeks. The severity of the illness is in relation to the amount of ingested neurotoxin. The epidemiologic study shows that all European cases were due to consumption of mussels from the Atlantic coast of Spain.

Adult↗