Transmission And Metabolism Of Paralytic Shellfish Poisoning In The Food Chain Of Marine Ecosystem

The transfer and transformation of paralytic shellfish poisoning are studied under laboratory controlled conditions, including the food chain from bivalve shellfish (Chlamys nobilis) to crustacean (Panulirus stimpsoni) and the food chain from dinoflagellate (Alexandrium tamarense) to cladoceran (Moina mongolica) and then to larval fish (Sciaenops ocellatus or Fugu rubripes). The ingesting of Moina mongolica on toxic A. tamarense and accumulation of PSP toxins by Moina mongolica are also researched when exposed to mixed-algae.The results showed as follows:Tansfer and transformation of PSP toxins occur when Panulirus stimpsoni fed with toxic viscera of Chlamys nobilis and depurated with non-toxic squid. In the whole experiment, only the hepatopancreas of lobster are detected out to contain paralytic shellfish poisoning, and the toxin profiles of which are the same as the viscera of scallop as carbamate toxins (GTX1.3), N-sulfocarbamoyl toxins (C1+2 and B₁) and decarbamoyl toxins (dcGTX₂₊₃). While differ from lobster, the α toxins dominate comparing with β toxins in the body of scallop. After consuming Chlamys nobilis for consecutive 6 days, Panulirus stimpsoni selectively accumulate the low toxicity N-sulfocarbamoyl toxins, and in the following process of depuration on non-toxic squid, N-sulfocarbamoyl toxins tend to converse into higher toxicity carbamate toxins. The content of dcGTX₂₊₃ decreased significantly and can't be detected out after 6 days cleanse, just because of their low accumulation concentration.Transmission and conversion of PSP toxins happen when Sciaenops ocellatus and Fugu rubripes prey on Moina mongolica that has ingested toxic Alexandrium tamarense ATCI01. All of them contain C₁₊₂ toxins,while viscera of Sciaenops ocellatus and Fugu rubripes create neoSTX toxin. β toxin (C₂) of C₁₊₂ toxins is predominant among dinoflagellate, cladoceran and larval fish, while the ratio of α toxin (C₁) to β toxin (C₂) in the larval fish is higher than that in the cladoceran. C₁₊₂ toxins of larval fish reduce remarkably in the course of depuration, and comparatively, neoSTX toxin don't show the same tendence.Toxic Alexandrium tamarense can be ingested by Moina mongolica in the mixed-algal food consisted of toxic A. tamarense and non-toxic Platymonas subcordiformis. When the concentration of A. tamarense is 430 cells ? ml/1, ingesting rate of Moina mongolica on A. tamarense and total toxin content don't change much regardless of density of P. subcordiformis. When the concentration of A. tamarense is 3970 cells ? mL"1, there is a negative correlation between ingesting rate and total toxin content. Toxin profiles both in Moina mongolica and A. tamarense are composed of C1+2 toxins. When the density of A. tamarense is 430 and 1920 cells ? mL"1, stereo isomer from C2 to Ci happen. While A. tamarense is 3970 cells ? mL"1, the degree of isomer was less than that in the tissue of A. tamarense. It implys that high concentration of dinoflagellate may do some harmful affects on the physiological activity of cladoceran.As a whole, this article indicates Panulirus stimpsoni, an important economic aquatic organism that is widespread along China seawater, may be contaminated by paralytic shellfish poison through preying on toxic shellfish in outdoor marine environment. Cladoceran, as well as copepod, can be a link/vector for PSP toxins flux in food webs and also be a sink for toxins by metabolizing and removing them from the environment. Larval fish, basis of fisheries industry, may be affected by PSP toxins because of its feeding on toxic zooplankton.