Page 304 - Algae
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Algae and Men                                                               287

                 epiphyte and has a relatively slow growth rate of approximately one division every 3 days. In its
                 coral reef habitat, G. toxicus is biflagellate and swims if disturbed, but is usually motionless and
                 attached to certain macroalgae. The dinoflagellate may also be associated with macroalgal detritus
                 on the sea floor. Some scientists believe that the diverse symptoms of CFP are a result of a com-
                 bination of several toxins or their metabolites, produced by one or more dinoflagellates.
                 However, G. toxicus, which is found on a variety of macroalgae eaten by herbivorous fish, is
                 now widely considered the single-celled source of ciguatoxins and the potential cause of CFP.
                     G. toxicus produces two classes of polyether toxins, the ciguatoxins (CTX) and maitotoxins
                 (MTX). The CTX are lipophilic and are accumulated in fish through food web transfer. More
                 than 20 CTX congeners have been isolated; however, only a few have been fully characterized
                 structurally. The maitotoxins are transfused ladder-like polyether toxins, but are somewhat more
                 polar, due to the presence of multiple sulfate groups. MTX was originally identified as a water
                 soluble toxin in the viscera of surgeonfishes, and later found to be the principal toxin produced
                 by G. toxicus. MTXs have not been demonstrated to bioaccumulate is fish tissues, possibly due
                 to their more polar structure. Thus, if MTX is involved in ciguatera poisoning, it may be implicated
                 only in ciguatera poisonings derived from herbivorous fishes.
                     The toxic potency of MTX exceeds that of CTX (respectively 10 ng/kg and 50 ng/kg in mice).
                 Its mode of action has not been fully elucidated. Its biological activity is strictly calcium dependent
                 and causes both membrane depolarization and calcium influx in many different cell types.
                     These toxins become progressively concentrated as they move up the food chain from small fish
                 to large fish that eat them, and reach particularly high concentrations in large predatory tropical reef
                 fish. Barracuda are commonly associated with ciguatoxin poisoning, but eating grouper, sea bass,
                 snapper, mullet, and a number of other fish that live in oceans between latitude 358N and 358S has
                 caused the disease. These fish are typically caught by sport fishermen on reefs in Hawaii, Guam and
                 other South Pacific islands, the Virgin Islands, and Puerto Rico. Ciguatoxin usually causes symp-
                 toms within a few minutes to 30 h after eating contaminated fish, and occasionally it may take up to
                 6 h. Common nonspecific symptoms include nausea, vomiting, diarrhea, cramps, excessive sweat-
                 ing, headache, and muscle aches. The sensation of burning or “pins-and-needles,” weakness,
                 itching, and dizziness can occur. Patients may experience reversal of temperature sensation
                 in their mouth (hot surfaces feeling cold and cold, hot), unusual taste sensations, nightmares, or
                 hallucinations. Ciguatera poisoning is rarely fatal. Symptoms usually clear in 1–4 weeks.
                     In its typical form, CFP is characterized initially by the onset of intense vomiting, diarrhoea,
                 and abdominal pain within hours of ingestion of toxic fish. Within 12–14 h of onset, a prominent
                 neurological disturbance develops, characterized by intense paraesthesia (tingling, crawling, or
                 burning sensation of the skin) and dysaesthesia (painful sensation) in the arms, legs, and perioral
                 region, myalgia, muscle cramping, and weakness. During this stage of the illness, pruritus and
                 sweating are commonly experienced.
                     Pseudonitzschia spp. are among the several other marine algae that can produce domoic acid,
                 the cause of ASP. Domoic acid was first isolated in Japan from the macroalgae species Chondria
                 armata in 1958, and was consequently called after the Japanese word for macroalgae, which is
                 domoi. Its identification in 1987 as a neurotoxin was first treated with scepticism, because this
                 water-soluble amino acid was known as a folk medicine in Japan to treat intestinal pinworm
                 infestations when used in very small doses. Production of domoic acid by algae seems to be a
                 genetic property for a secondary metabolite with no known function in defence or primary
                 metabolism.
                     Domoic acid can enter the marine food chain via uptake by molluscan shellfish such as
                 mussels that filter their food out of the water. This water can contain both diatoms and the
                 toxin, which is released to the water column (although there is no evidence yet that the toxin
                 can be taken up directly). The toxin accumulates in the digestive gland and certain tissues of
                 shellfish, and it appears to have no effect on the animals. Domoic acid may be metabolized
                 by bacteria (e.g., of the genera Alteromonas and Pseudomonas) present in tissue of blue
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