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Electron capture gas chromatographic determination of Kepone residues in environmental samples.

The pollution of the environment with Kepone (decachlorooctahydro-1,3,4-metheno-2H-cyclobuta[cd]pentalen-2-one) by an industrial manufacturer of the pesticide resulted in the contamination of several terrestrial media, including biological life, near the entry of the insecticide into the ecosystem. The substrata investigated and for which residue methodology was developed included river sediment, soil, water, shellfish, and finfish. Rigorous extraction techniques utilizing the Soxhlet apparatus and the Polytron tissue homogenizer were required for complete removal of Kepone from the samples. Finfish tissue was the most difficult to analyze. For this type of substratum, a preliminary cleanup by gel permeation chromatography was required to remove most of the lipid material followed by a micro Florisil column elution to eliminate polychlorinated biphenyls (PCB'S). Cleanup of shellfish and other environmental samples was accomplished with a micro Florisil column only. Electron capture gas chromatography was used to analyze the sample extracts. Recoveries of Kepone from fortified samples averaged 84% or greater.

Animals↗

Nondestructive neutron activation analysis of marine organisms collected from ocean dump sites of the middle eastern United States.

The concentrations of eight metals were determined by a nondestructive neutron activation technique for eleven species of fish and shellfish. The marine organisms were collected from ocean dump sites off New York City, off New Haven, Connecticut, and off Delaware Bay. Antimony was not detected in most of the organisms examined in thid study; the detection limit was about 0.02 to 0.05 ppm. Antimony levels ranged from 0.01 to 0.129 ppm in fish that had detectable levels. Cobalt levels were low in all samples with most levels in the range of 0.1 to 0.3 ppm. Chromium concentrations at 0.3 to 1.0 ppm were only roughly quantitated by the procedure employed. Most marine organisms examined had chromium levels at or below these values. Nickel was not detected in any of the organisms examined; the detection limit was in the 3 to 6 ppm range. Rubidium concentrations were 0.6 to 1.5 ppm for most organisms; only rough quantitative measurement was possible at these levels. Selenium levels ranged from about 0.3 to 3.8 ppm in all samples. Silver concentrations were below 0.3 ppm in most organisms. Silver concentrations as high as 10 to 30 ppm, however, were found in the digestive gland of rock crab. Zinc levels in windowpane flounder liver were about 6 to 9 times greater than the 4 to 10 ppm levels found in muscle. Zinc concentrations in rock crab muscle, on the other hand, were only slightly higher than the 15 to 32 ppm concentration found in the digestive gland. Fish other than windowpane flounder had zinc levels that ranged from 4 to 9 ppm in the muscle and 14 to 42 ppm in the liver. Shellfish other than rock crab had zinc levels of 15 to 30 ppm in muscle and 17 to 40 ppm in the digestive gland.

Animals↗

Potential for employing the distribution of anomalous non-methylene-interrupted dienoic fatty acids in several marine invertebrates as part of food web studies.

A group of homologous, nonmethylene-interrupted dienoic fatty acids (NMID) recently reported in oysters has been found in several other shellfish species and also in other marine phyla. The distribution of most other "normal" fatty acids among several species of shellfish is basically similar but mantle lipids from two other molluscan species, both squid, differ radically. The squid mantle fatty acids do not include NMID, suggesting that in molluscs NMID may accumula-e primarily in filter-feeders or herbovores. The distribution of these anomalous fatty acid components in higher species suggests that they reflect invertebrates in the diet and are biochemically inert.

Animals↗

Adaptive response to cold temperatures in Vibrio vulnificus.

The effectiveness of rapid chilling or freezing of oysters to reduce Vibrio vulnificus levels in shellfish may be compromised by product handling procedures that permit cold adaptation. When a V. vulnificus culture was shifted from 35 degrees C to 6 degrees C conditions, it underwent transition to a non-culturable state. Cells adapted to 15 degrees C prior to change to 6 degrees C condition, however, remain viable and culturable. In addition, cultures adapted to 15 degrees C were able to survive better upon freezing at -78 degrees C compared with cultures frozen directly from 35 degrees C. Inhibition of protein synthesis by addition of chloramphenicol in a V. vulnificus culture immediately prior to the exposure to the adaptive temperature eliminated inducible cold tolerance. These results suggest that cold-adaptive "protective" proteins may enhance survival and tolerance at cold temperatures. In addition, removal of iron from the growth medium by adding 2,2'-Dipyridyl prior to cold adaptation decreased the viability by approximately 2 logarithm levels. This suggests that iron plays an important role in adaptation at cold temperatures. Analysis of total cellular proteins on an SDS polyacrylamide gel electrophoresis, labeled with 35S-methionine during exposure at 15 degrees C, showed elevated expressions of a 6-kDa and a 40-kDa protein and decreased expression of an 80-kDa protein. These results suggest that, for V. vulnificus, survival and tolerance at cold temperatures could be due to the expression of cold-adaptive proteins other than previously documented major cold shock proteins such as CS7.4 and CsdA. In this study, for the first time we have shown that exposure to an intermediate cold temperature (15 degrees C) causes a cold adaptive response, helping this pathogen remain in culturable state when exposed to a much colder temperature (6 degrees C). This adaptive nature to cold temperatures could be important for shellfish industry efforts to reduce the risk of V. vulnificus infection from consuming raw oysters.

Adaptation, Physiological↗

The effect of brevenal on brevetoxin-induced DNA damage in human lymphocytes.

Brevenal is a nontoxic short-chain trans-syn polyether that competes with brevetoxin (PbTx) for the active site on voltage-sensitive sodium channels. The PbTxs are highly potent polyether toxins produced during blooms of several species of marine dinoflagellates, most notably Karenia brevis. Blooms of K. brevis have been associated with massive fish kills, marine mammal poisoning, and are potentially responsible for adverse human health effects such as respiratory irritation and airway constriction in beach-goers. Additionally, the consumption of shellfish contaminated with PbTxs results in neurotoxic shellfish poisoning (NSP). The purpose of the present study was to determine whether PbTx could induce DNA damage in a human cell type, the lymphocyte, and if so, whether the damage could be antagonized or ameliorated by brevenal, a brevetoxin antagonist. The DNA damage may occur through both endogenous and exogenous physiological and pathophysiological processes. Unrepaired or erroneously repaired DNA damage may result in gene mutation, chromosome aberration, and modulation of gene regulation, which have been associated with immunotoxicity and carcinogenesis. A single-cell gel electrophoresis assay, or comet assay, was used to determine and compare DNA damage following various treatments. The data were expressed as tail moments, which is the percentage of DNA in the tail multiplied by the length between the center of the head and center of the tail (in arbitrary units). The negative control tail moment was 29.2 (SE=+/-0.9), whereas the positive control (hydrogen peroxide) was 72.1 (1.5) and solvent (ethanol) was 24.2 (2.1). The PbTx-2 (from Sigma, St. Louis, MO, USA), 10(-8) M was 41.3 (3.6), PbTx-9 (Sigma), 10(-8) M was 57.0 (5.3), PbTx-2 (from University of North Carolina at Wilmington, UNCW), 10(-8) M was 49.4 (9.9), and PbTx-3 (UNCW), 10(-8) M was 64.0 (6.4). 1.0 microg/ml brevenal applied 1 h before the PbTxs protected the lymphocytes from DNA damage; PbTx-2 (Sigma), 31.3 (2.1); PbTx-9 (Sigma), 35.5 (2.9); PbTx-2 (UNCW), 33.9 (1.4); PbTx-3 (UNCW), 34.9 (1.25). The tail moment for 1.0 mug/ml brevenal alone was 30.8 (2.6). The results indicate that extensive genotoxic damage is induced by PbTx-2 and 9 (Sigma), and PbTx-2 and 3 (UNCW) in normal human lymphocytes, which is fully antagonized by brevenal. This suggests that the immune systems of individuals exposed to PbTx during harmful algal bloom (HAB) events may be at risk.

Animals↗

DNA breaks and cell cycle arrest induced by okadaic acid in Caco-2 cells, a human colonic epithelial cell line.

Okadaic acid (OA) is a shellfish toxin produced by dinoflagellates, in mussels. It is a potent tumour promoter and represents a potential threat to human health even at low concentrations. OA targets mainly the gastrointestinal tract in acute poisoning, causing diarrhoea. Therefore the present investigations were designed to study the ability of okadaic acid to induce cytotoxicity and DNA lesions in a human colonic cell line (Caco-2). Incubation of Caco-2 cells with OA (3.75-60 ng/ml, i.e. 4.6 x 10(-3)-7.5 x 10(-2) microM) causes a significant reduction in cell viability. Moreover, okadaic acid inhibits protein and DNA synthesis with, respectively, IC50 of 16 and 6.5 ng/ml after 24 h incubation. It also provokes cell cycle arrest, characterised by an increase in the number of S phase cells, correlated with a significant decrease in G0/G1 phase cells at high concentration. One of the main results obtained in these investigations is the apoptosis induced by OA in Caco-2 cells of intestinal origin, shown by DNA laddering in agarose gel electrophoresis (250-1000 base pairs). OA also induces clastogenic effects evaluated by DNA fragmentation analysis using the method of Higuchi and Aggarwal (52% for 60 ng/ml) and comet assay (increase of the frequency of comets and their tails length). Therefore, the cell death induced by OA seems clearly to be concentration-dependent after 24 h of incubation. The cytotoxic properties of okadaic acid and its ability to damage DNA result in cell death, mainly by apoptosis. Since consumption of shellfish contaminated with acceptable okadaic acid concentrations exposes colonic cells to harmful concentrations of this toxin, the possibility that OA would display its toxic effects on intestinal cells in vivo should be evaluated in human primary intestinal cells and human intestinal slices for cytotoxic effects, DNA fragmentation and apoptosis.

Caco-2 Cells↗

Comparison of different fluorimetric HPLC methods for analysis of acidic polyether toxins in marine phytoplankton.

The human toxic syndrome, diarrhetic shellfish poisoning (DSP), is caused by polyether toxins that are present in bivalve molluscs but originate from some species of marine phytoplankton. During the last few years different HPLC methods with fluorescence detection (FLD) have been proposed for analysis of marine toxins, including polyether toxins, in shellfish and phytoplankton. Several derivatization reagents have been proposed in the literature, with the aim of converting the acidic DSP toxins into their corresponding fluorescent derivatives. In this work we report results obtained from HPLC-FLD analysis of extracts from phytoplankton, including Dinophysis spp.,harvested off the south-west coast of Ireland. Three different reagents were used for fluorescent derivatization: 3-bromomethyl-6,7-dimethoxy-1-methyl-2(1H)-quinoxalinone (BrDMEQ), 9-chloromethylanthracene (CA), and "in situ" 9-anthracenyldiazomethane (ADAM). Derivatization was performed under conditions previously optimised. The DSP derivatives were cleaned using different SPE procedures then analysed by HPLC-FLD. In this study, the use of BrDMEQ, CA, and "in situ" ADAM was compared in terms of sensitivity and selectivity. Evaluation of HPLC methods for analysis of DSP toxin derivatives was also conducted; the presence of okadaic acid (OA), dinophysistoxin-2 (DTX-2), and pectenotoxin-2 seco acids (PTX1SAs) was detected in the sample extracts studied.

Animals↗

Detection of domoic acid in rat serum and brain by direct competitive enzyme-linked immunosorbent assay (cELISA).

In 1987 a large-scale incident of human poisoning in Canada was traced to commercial mussels contaminated with domoic acid (DOM). Since then, routine screening of shellfish domoic acid content has been carried out using a variety of assays, with liquid chromatography using ultraviolet absorbance detection (LC-UV) or mass spectrometric detection (LC-MS) being the currently accepted standard methodologies. Recently, a highly specific competitive enzyme-linked immunosorbent assay (cELISA) has been developed for the detection and analysis of DOM in commercial shellfish, but its accuracy relative to LC methods has not been independently verified in mammalian tissues. In this study we demonstrate that measurement of rat serum DOM concentration by cELISA gives a good correlation (r2 = 0.993) across a broad range of concentrations when compared to LC-MS analysis, with only a small (15%) overestimation of sample DOM content. In addition, we have developed an extraction method for analysis of DOM in rat brain by cELISA which yields complete recovery across a range of sample dilutions.

Animals↗

Survival of Cryptosporidium parvum oocysts recovered from experimentally contaminated oysters (Ostrea edulis) and clams (Tapes decussatus).

Samples of two species of shellfish that form part of the human food chain (the oyster Ostrea edulis and the marine clam Tapes decussatus) were experimentally contaminated with Cryptosporidium parvum oocysts. Changes in the viability of oocysts subsequently recovered from the shellfish were evaluated by means of an immunofluorescent antibody technique (IFAT) and inclusion/exclusion of the fluorogenic vital dye propidium iodide. There was a sharp decrease in oocyst viability during the first 4 days, with 15-25% viable oocysts remaining thereafter. In addition the infectivity of these oocysts at 10 and 31 days post-contamination was demonstrated using a suckling murine model.

Animals↗

Vibrio cholerae O2 sepsis in a patient with AIDS.

Vibrio cholerae strains other than O1 and 0139 (non-O1 Vibrio cholerae) are associated with sporadic diarrheal disorders and limited outbreaks of diarrhea and have often been reported in association with extraintestinal infections. The following is a presentation of a fatal case of non-O1 Vibrio cholerae septicemia with disseminated intravascular coagulation and cutaneous bullous lesions that occurred in a patient infected with the acquired immunodeficiency syndrome. In order to prevent Vibrio cholerae infection, patients with underlying diseases should be warned of the risk factors for acquiring such infection, including consumption of raw shellfish and exposure to sea and fresh water where shellfish are found.

Acquired Immunodeficiency Syndrome↗

Marine Neurotoxins: Ingestible Toxins.

Fish and shellfish account for a significant portion of food-borne illnesses throughout the world. In general, three classes of diseases result from seafood consumption--intoxication, allergies, and infections. In this review, the authors discuss several seafood-borne toxins, including domoic acid, which acts on the central nervous system. In addition, the authors discuss ciguatoxin-, brevetoxin-, saxitoxin-, tetrodotoxin-, and scombroid-related histamine toxicity, all of which act primarily on the peripheral nervous system. Fish has become a very popular food in the US mostly related to its potential health benefits. Fish is consumed to such a degree that fishing stocks are reportedly at an all time low from what seemed like an endless supply even 30 years ago. One of the most significant threats to human intoxication is the recreational harvest of shellfish, often times located in remote locations where the harvesters are subsistent on fishery resources and have no monitoring in place. The hazard to intoxication is not as common in purchased seafood, which is more stringently regulated, yet still is a serious problem. Most ingestible toxins are thermo-stable and therefore unaffected by cooking, freezing, or salting. Air transport of consumable products throughout the world makes it easy to obtain exotic edibles from far away countries. A seemingly unusual toxin can be more commonly encountered than previously thought and it is important to consider this when evaluating patients. Recognition and treatment of various neurologic symptoms related to seafood ingestion is paramount in today's mobile, gastronomic world. Specific treatments vary with each individual toxin and with the individual's specific reaction to the toxin. Generally, some degree of medical care is required with all ingestible toxin exposure, ranging from simple administration of medication and hydration to ventilatory and cardiovascular support.

Journal Article↗

Enzymatic transformation of PSP toxins in the littleneck clam (Protothaca staminea).

Stemming from investigations into the relationship between toxins produced by Gonyaulax sp. and accumulated in shellfish, we wish to report enzymatic transformations of the PSP toxins to decarbamoyl derivatives in the littleneck clam (Protothaca staminea). No toxin transformations were observed in either mussels (Mytilus edulis) or in butter clams (Saxidomus giganteus). In addition, littleneck clam samples from the natural environment contained predominantly the decarbamoyl derivatives, while other shellfish species collected from the same vicinity contained the previously reported PSP toxins.

Animals↗

Ozone depuration of Vibrio vulnificus from the southern quahog clam, Mercenaria campechiensis.

Southern quahog clams, Mercenaria campechiensis, were dosed with Vibrio vulnificus and placed in a pilot-scale depuration system using ozonated recirculated artificial seawater. Twenty-four hours of treatment with ozone-treated recirculating artificial seawater reduced the numbers of V. vulnificus in the shellfish meats by an average of 2 log units when compared to natural die-off in control clams. The oxidant levels (up to 3 mg/liter) did not adversely affect shellfish pumping during the depuration process.

Animals↗

Disorders of neuromuscular transmission due to natural environmental toxins.

A variety of natural toxins of animal, plant, and bacterial origin are capable of causing disorders of neuromuscular transmission. Animal toxins include venomous snakes and arthropods, venoms of certain marine creatures, skin secretions of dart-poison frogs, and poisonous fish, shellfish, and crabs. There are plant poisons such as curare, and bacterial poisons such as botulinum toxin. These act at single or multiple sites of the neuromuscular apparatus interfering with voltage-gated ion channels, acetylcholine release, depolarization of the postsynaptic membrane, or generation and spread of the muscle action potential. The specific actions of these toxins are being widely exploited in the study of neuromuscular physiology and pathology. Some toxins have proved to be valuable pharmaceutical agents. Poisoning by natural neurotoxins is an important public health hazard in many parts of the world, particularly in the tropics. Poisoning may occur by a bite or a sting of a venomous animal, or by the ingestion of poisonous fish, shellfish or other marine delicacies. Contaminated food is a vehicle for poisons such as botulinum toxin. Clinically, a cardinal feature in the symptomatology is muscle paralysis with a distribution characteristic of myasthenia gravis, affecting muscles innervated by cranial nerves, neck flexors, proximal limb muscles, and respiratory muscles. Respiratory paralysis may end fatally. This paper reviews from the clinical and pathophysiologic viewpoints, naturally occurring environmental neurotoxins acting at the neuromuscular junction.

Animals↗

Histopathological studies on experimental marine toxin poisoning. I. Ultrastructural changes in the small intestine and liver of suckling mice induced by dinophysistoxin-1 and pectenotoxin-1.

Sequential ultrastructural changes were studied in mouse digestive organs after i.p. injections of dinophysistoxin-1 and pectenotoxin-1, causative agents of diarrhetic shellfish poisoning. Dinophysistoxin-1, a diarrheagenic substance, produced severe mucosal injuries in the small intestine within 1 hr after the administration of the toxin. The injuries were divided into 3 consecutive stages: extravasation of villi vessels, degeneration of absorptive epithelium and desquamation of the degenerated epithelium from the lamina propria. In contrast to dinophysistoxin-1, pectenotoxin-1, a non-diarrheagenic toxin from diarrhetic shellfish poisoning causative mussels, resulted in no abnormalities in the small intestine, but did cause characteristic liver injuries. Within 1 hr after the injection of pectenotoxin-1 numerous non-fatty vacuoles appeared in the hepatocytes around the periportal regions of the hepatic lobules. Electron microscopic observations with colloidal iron demonstrated that these vacuoles originated from invaginated plasma membranes of the hepatocytes.

Animals↗

Respiratory effects of brevetoxin and saxitoxin in awake guinea pigs.

Ptychodiscus brevis toxin (brevetoxin) is associated with 'Florida red tide' and cause neurotoxic shellfish poisoning. Saxitoxin is the agent of paralytic shellfish poisoning. Clinical reports of human intoxication suggest that both toxins affect the respiratory system. The toxins were administered by slow intravenous infusion. The effects of the toxins on respiratory function of awake guinea pigs in a pressure plethysmograph were studied. Both toxins caused lactic acidosis of unknown etiology, which was compensated for by increased minute volume with brevetoxin (PbTx-3)- but not with saxitoxin-intoxicated animals. In general, brevetoxin increased ventilation, before respiratory failure, while saxitoxin had a depressive effect on ventilation. Airways resistance was not increased, nor was dynamic compliance decreased during intoxication, although the data suggest that respiratory system failure was the primary cause of death. The responses seen in these experiments are consistent with the dissimilar molecular actions of these toxins.

Animals↗

Preparation of monoclonal antibodies against okadaic acid prepared from the sponge Halichondria okadai.

Three murine monoclonal antibodies, OA-1, OA-2 and OA-3, against okadaic acid were prepared from hybridoma clones obtained by fusion of mouse 653 myeloma cells with mouse immune spleen cells sensitized to okadaic acid-ovalbumin conjugate. Each antibody reacted with dinophysistoxin-1 ( = 35-methylokadaic acid) as well as okadaic acid, but did not react with the other diarrhetic shellfish poisons or related compounds, such as 7-O-palmitoyl-okadaic acid (analogue of dinophysistoxin-3), pectenotoxin-1 and yessotoxin. A competitive inhibition enzymelinked immunosorbent assay which employed OA-3 antibody was performed and showed a sensitivity of about 10 ppb (10 ng/ml) for okadaic acid. This simple and time-saving ELISA assay system may be useful for the specific detection of diarrhetic shellfish poisons.

Animals↗

Tetrodotoxin secretion from the lined moon shell Natica lineata in response to external stimulation.

The lined moon shell Natica lineata secretes tetrodotoxin (TTX) in response to an external stimulation such as removal from the seawater. The toxin released from the shellfish contained 14-361 mouse units of TTX per specimen. The shellfish did not secrete any further toxin when seawater removal was repeated over four times at about 1 hr intervals. All specimens recovered TTX secreting ability when they were kept in an aquarium for 5 days.

Animals↗