The Toxin of the Marine Alga Prymnesium Patelliferum Increases Cytosolic Ca²⁺ in Synaptosomes and Voltage Sensitive Ca²⁺-Currents in Cultured Pituitary Cells

Abstract

During the last four years the closely related ichthyotoxic marine flagellates Prymnesium patelliferum and Prymnesium parvum have appeared in blooms in the brackish waters in the fjords of south-western Norway. The algal blooms have caused the death of large amounts of salmon and rainbow trout in fish farms (varying between 150–750 metric tons per year). In highly toxic blooms the fish die within 5–30 minutes after spasmodic movements. The precise mechanism of action of the algal toxin is not clear although the gills seems to be the primary organ affected (Shilo, 1971). Studies have been carried out on various biological test systems, and in the litterature the effects of the Prymnesium-toxin is divided into four categories: ichthyotoxic effects, hemolytic effects, cytotoxic effects and neurotoxic effects (Yariv and Hestrin, 1961; Dafni and Giberman, 1971; Parnas and Abbott, 1965); which are all results of interaction with biological membranes. Addition of high doses of toxin for prolonged periods leads to membrane lysis. Using liposomes Imai and Inoue (1974) found that the amount of toxin required for lysis increased with decreasing content of cholesterol in the membrane. Furthermore, the net charge of the liposome membrane was not important for the interaction with the algal toxin. The chemical structure of the algal toxin is not yet fully described, and it is not clear whether the observed effects are due to one or several toxin components. A substance of P.parvum screened for its hemolytic activity has been isolated and identified as a mixture of two polar digalactomonoglycerides: 1'-O-octadecatetraenoyl-3'-O-(6-O-β-Dgalactopyranosyl-β-D-galactopyranosyl)-glycerol and 1'-O-octadecapentaenoyl-3'-O-(6-O-β-D-galactopyranosyl-β-D-galactopyranosyl)-glycerol (Kozakai et al, 1982).