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Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart arrhythmia, and changing the senses of heat and cold. Such poisoning from ciguatoxins is known as ciguatera.
[6] [21] [22] [23] Ciguatoxin lowers the threshold for opening voltage-gated sodium channels in synapses of the nervous system. Opening a sodium channel causes depolarization, which could sequentially cause paralysis, heart contraction, and changing the senses of hot and cold.
Ciguatoxin 1 or CTX-1 is a toxic chemical compound, the most common and potent type in the group of ciguatoxins. It is a large molecule consisting of polycyclic polyethers that can be found in certain types of fish in the Pacific Ocean. The compound is produced by Dinoflagellates Gambierdiscus toxicus and is passed on through the food chain by ...
Gambierdiscus toxicus is a species of photosynthetic unicellular eukaryote belonging to the Alveolata, part of the SAR supergroup.It is a dinoflagellate which can cause the foodborne illness ciguatera, [1] and is known to produce several natural polyethers including ciguatoxin, maitotoxin, gambieric acid, and gambierol.
Several Gambierdicus species produce potent toxin such as ciguatoxin and maitotoxin, which cause ciguatera fish poisoning. [4] Humans often consume the toxins, as herbivorous fish, which feed on macroalgae, ingest the dinoflagellates. Afterwards, carnivorous fish, which are targeted by fishing industries, move the toxins further up the food chain.
Scaritoxin, a potent toxic substance, is a ciguatoxin with molecular formula C 60 H 84 O 16. [1] Scaritoxin is also referred to as ciguaotoxin 4A, CTX4A. [1] Like other ciguatoxins, CTX4A is produced by dinoflagellate Gambierdiscus toxicus and isolated from poisonous fish.
This results in neuroexcitation, membrane depolarization, and spontaneous nerve firing. Brevetoxins are a group of greater than ten lipid-soluble cyclic polyethers that bind to a specific site on the voltage-gated sodium channel (VGSC) , leading to an influx of sodium ions into the cell.
Cicutoxin binds to the same place as GABA, because of this the receptor is not activated by GABA. The pore of the receptor won't open and chloride can't flow across the membrane. Binding of cicutoxin to the beta domain also blocks the chloride channel. Both effects of cicutoxin on the GABA A-receptor cause a constant depolarization.