Contraction of the muscle takes by the opening of voltage gated sodium channels. The toxin produced by the fish called cinguatoixns have been bind to and modulate the activity of cell membrane voltage gated sodium channels.Cinguatoxins binds at site 5 on the alpha subunit resulting in the opening of the channnles at resting membrane potential. Sodium influx causes membrane depolarization and spontaneous or repetitive firing of action potentials. The neuroexcitability might result in the increased recovery of sodium chnnaels. The influx of the sodium into the neuronal tissue results in cellular swelling with decreases conduction velocity and neurotransmmison. This excess neuroexcitation is thought to be the etiology of the neurological symptoms of ten described by the patients.
Symptoms typically appear within the initial 8 hours following ingestion of toxic fish, followed over the subsequent 10 to 18 hours by headache, myalgias, and loss of tendon reflexes.By 24 hours, sensory symptoms predominant, manifested by perioral and limb paresthesias, dysesthesis, and pruritus. These sensory symptoms gradually evolve over the ensuing 2 to 5 days into paradoxical sensory disturbances, such as feeling heat as cold, and vice versa. Such paradoxical sensory perceptions are the clinical hallmark of CTX but may also occur with some shellfish toxins associated with red tide.
When administered it might result in the cardiovascular problems, hyperventilation at low doses and at high doses it might result in depression of the respiratory system. Atrioventricular conduction abnormalities at low dpses, with arrythmias and ventricular tachycardia with transient hypertension at sublethal doses, and falling arterial pressure and result in complete heart failure at high doses.
High dose of cinguatoxins might result in the cardiac arrhythmias and an increase in contractability which are followed by a fall in cardiac contractibility coupled and a lidocaine sensitive change in membrane depolarization.
The blue-green and free algal dinoflagellate Gambierdiscus toxicus is the main agent ciguatoxins. G. toxicus adheres to dead coral surfaces and marine algae that are consumed by smaller herbivorous fish. Although G. toxicus is very likely responsible for the majority of ciguatoxins encountered in fish, the cyanobacterium Trichodesmium erythraeum can produce precursors to the toxins that may generate ciguatera syndrome. Other dinoflagellates may also generate toxins that play a role in ciguatera syndrome. Larger reef fish eat the contaminated smaller fish, thereby becoming vectors, as ciguatoxin is bioconcentrated up the food chain. It has long been assumed that smaller fish within a given species are safer to eat than the larger ones.. Although the entire fish is toxic, the viscera (particularly the liver) and roe are considered to carry the highest concentrations of toxin.
Three major ciguatoxins (CTX-1, CTX-2, and CTX-3) are usually found in the flesh and viscera of ciguateric fishes. Each is found in variable concentrations, which may account for inconsistency of reported clinical signs and symptoms. Ciguatoxins are potent Na+ channel toxins and exert their effects by activating voltage-sensitive Na+ channels. The Na channels open at resting membrane potentials, leading to spontaneous firing of neurons, giving rise to the neurologic signs and symptoms of ciguatera. Electrophysiologic studies of the sural and common peroneal nerves in humans with ciguatera, demonstrating reduced light touch, pain, and vibratory sensation in the extremities, showed prolongation of the absolute refractory, relative refractory, and supernormal periods. These findings indirectly suggest that CTX may abnormally prolong sodium channel opening in nerve membranes.
All identified toxins associated with ciguatera are unaffected by freeze-drying, heat, cold, and gastric acid and do not affect the odor, color, or taste of the fish. There is some evidence that cooking methods can alter the relative concentrations of the various toxins. For example, boiling fish flesh will remove water-soluble toxins, but frying or grilling the flesh may increase toxicity of lipid-soluble toxins as a result of releasing lipid-soluble components from the cellular compounds to which they are normally bound.