domoic-acid and Amnesia

domoic-acid has been researched along with Amnesia* in 7 studies

Reviews

2 review(s) available for domoic-acid and Amnesia

ArticleYear
Domoic acid epileptic disease.
    Marine drugs, 2014, Mar-06, Volume: 12, Issue:3

    Domoic acid epileptic disease is characterized by spontaneous recurrent seizures weeks to months after domoic acid exposure. The potential for this disease was first recognized in a human case study of temporal lobe epilepsy after the 1987 amnesic shellfish-poisoning event in Quebec, and was characterized as a chronic epileptic syndrome in California sea lions through investigation of a series of domoic acid poisoning cases between 1998 and 2006. The sea lion study provided a breadth of insight into clinical presentations, unusual behaviors, brain pathology, and epidemiology. A rat model that replicates key observations of the chronic epileptic syndrome in sea lions has been applied to identify the progression of the epileptic disease state, its relationship to behavioral manifestations, and to define the neural systems involved in these behavioral disorders. Here, we present the concept of domoic acid epileptic disease as a delayed manifestation of domoic acid poisoning and review the state of knowledge for this disease state in affected humans and sea lions. We discuss causative mechanisms and neural underpinnings of disease maturation revealed by the rat model to present the concept for olfactory origin of an epileptic disease; triggered in dendodendritic synapases of the olfactory bulb and maturing in the olfactory cortex. We conclude with updated information on populations at risk, medical diagnosis, treatment, and prognosis.

    Topics: Aged; Aged, 80 and over; Aging; Amnesia; Animal Diseases; Animals; Behavior, Animal; Bivalvia; Epilepsy; Epilepsy, Temporal Lobe; Female; Food Contamination; Hippocampus; Humans; Kainic Acid; Male; Marine Toxins; Middle Aged; Neuromuscular Depolarizing Agents; Neurotoxins; Olfactory Pathways; Rats; Recurrence; Sea Lions; Seizures; Shellfish Poisoning

2014
Amnesic shellfish poison.
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2004, Volume: 42, Issue:4

    Amnesic shellfish poisoning (ASP) is caused by consumption of shellfish that have accumulated domoic acid, a neurotoxin produced by some strains of phytoplankton. The neurotoxic properties of domoic acid result in neuronal degeneration and necrosis in specific regions of the hippocampus. A serious outbreak of ASP occurred in Canada in 1987 and involved 150 reported cases, 19 hospitalisations and 4 deaths after consumption of contaminated mussels. Symptoms ranged from gastrointestinal disturbances, to neurotoxic effects such as hallucinations, memory loss and coma. Monitoring programmes are in place in numerous countries worldwide and closures of shellfish harvesting areas occur when domoic acid concentrations exceed regulatory limits. This paper reviews the chemistry, sources, metabolism and toxicology of domoic acid as well as human case reports of ASP and discusses a possible mechanism of toxicity.

    Topics: Amnesia; Animals; Disease Outbreaks; Foodborne Diseases; Humans; Kainic Acid; Marine Toxins; Mollusca; Neurotoxins; Shellfish

2004

Other Studies

5 other study(ies) available for domoic-acid and Amnesia

ArticleYear
Beware of amnesic shellfish poisoning.
    Nursing, 2017, Volume: 47, Issue:7

    Topics: Amnesia; Animals; Bivalvia; Emergency Nursing; Humans; Kainic Acid; Nursing Diagnosis; Nursing Staff, Hospital; Shellfish Poisoning

2017
Amnesic shellfish poisoning toxin stimulates the transcription of CYP1A possibly through AHR and ARNT in the liver of red sea bream Pagrus major.
    Marine pollution bulletin, 2009, Volume: 58, Issue:11

    To investigate the role of detoxification-related liver genes in amnesic shellfish poisoning toxin metabolism, red sea bream Pagrus major were exposed to domoic acid (DA, 2mugg(-1) wet weight) for 24h. Hepatic mRNA expression levels of AHR, ARNT, CYP1 and GSTs were determined by semi-quantitative RT-PCR. The cytosolic factors aryl hydrocarbon receptor (AHR) and aryl hydrocarbon receptor nuclear translocator (ARNT) mRNA levels of DA exposure group were substantially enhanced by 113.3% and 90.9%, respectively. Consistent with this result, the phase I xenobiotic metabolizing enzyme (XME) cytochrome P-450 1A (CYP1A) was significantly induced. In contrast, the transcriptions of three major phase II XME glutathione S-transferases as well as heat shock protein 70 were not significantly affected by DA exposure. These results suggest a possible role of CYP1A after DA exposure in the toxin metabolism of marine fish, possibly through the AHR/ARNT signaling pathway.

    Topics: Amnesia; Animals; Aryl Hydrocarbon Receptor Nuclear Translocator; Cloning, Molecular; Cytochrome P-450 CYP1A1; Kainic Acid; Liver; Marine Toxins; Phylogeny; Receptors, Aryl Hydrocarbon; RNA, Messenger; Sea Bream; Shellfish Poisoning; Transcription Factors; Transcription, Genetic

2009
Environmental and health effects associated with Harmful Algal Bloom and marine algal toxins in China.
    Biomedical and environmental sciences : BES, 2004, Volume: 17, Issue:2

    The frequency and scale of Harmful Algal Bloom (HAB) and marine algal toxin incidents have been increasing and spreading in the past two decades, causing damages to the marine environment and threatening human life through contaminated seafood. To better understand the effect of HAB and marine algal toxins on marine environment and human health in China, this paper overviews HAB occurrence and marine algal toxin incidents, as well as their environmental and health effects in this country. HAB has been increasing rapidly along the Chinese coast since the 1970s, and at least 512 documented HAB events have occurred from 1952 to 2002 in the Chinese mainland. It has been found that PSP and DSP toxins are distributed widely along both the northern and southern Chinese coasts. The HAB and marine algal toxin events during the 1990s in China were summarized, showing that the HAB and algal toxins resulted in great damages to local fisheries, marine culture, quality of marine environment, and human health. Therefore, to protect the coastal environment and human health, attention to HAB and marine algal toxins is urgently needed from the environmental and epidemiological view.

    Topics: Amnesia; Animals; China; Ciguatoxins; Diarrhea; Dinoflagellida; Environment; Eukaryota; Eutrophication; Fisheries; Food Contamination; Foodborne Diseases; Humans; Kainic Acid; Lethal Dose 50; Marine Toxins; Neurotoxicity Syndromes; Okadaic Acid; Oxocins; Paralysis; Seawater; Shellfish Poisoning

2004
Amnesic shellfish poisoning: a new clinical syndrome due to domoic acid.
    Canada diseases weekly report = Rapport hebdomadaire des maladies au Canada, 1990, Volume: 16 Suppl 1E

    Topics: Adult; Amnesia; Animals; Bivalvia; Canada; Disease Outbreaks; Female; Humans; Kainic Acid; Male; Marine Toxins; Middle Aged; Neurotoxins; Shellfish Poisoning

1990
Domoic acid, an environmental toxin, produces hippocampal damage and severe memory impairment.
    Neuroscience letters, 1990, Dec-11, Volume: 120, Issue:2

    Microinjections of domoic acid, a presumed shellfish toxin, into the hippocampal formation of rats produces degeneration of CA3 and CA1 pyramidal cells and dentate gyrus granule cells. We demonstrate that domoate-treated rats exhibit a long-lasting anterograde amnesia for spatial information in the Morris water task. This preparation provides a good model for examining neurotoxicity and the anterograde amnesic syndrome observed in humans following consumption of domoate-contaminated shellfish.

    Topics: Amnesia; Animals; Hippocampus; Kainic Acid; Male; Memory; Neurotoxins; Pyramidal Tracts; Rats; Rats, Inbred Strains; Space Perception

1990