Hemolytic activity of the nematocyst venom from the sea anemone Bundodosoma Caissarum

The nematocyst venom of the sea anemone Bunodosoma caisarum obtained by electric stimulation of the animals has hemolytic activity on fish, toad, snake, mice and rat erythrocytes. The hemolytic action was dose-dependent and the ED50 varied between 2.9 and 7.6*g venom/ml erythrocyte suspension (0.5%, v/v). Toad erythrocytes were the most sensitive while rat erythrocytes were the most resistant to the sea anemone venom. The hemolytic activity of venom in mice was partially inhibited by preincubation of the venom with sphingomyelin for 1h. The ED50 was increased 3.8-fold when 10.0* sphingomyelin per ml erythrocyte suspension produced approximately 95% hemolysis and were inhibited only by 40.0*g sphingomyelin. The hemolysin activity was inhibited by heating to 90-C but not to 70-C

Photosensitization of cultured cells and viruses by pyrene lipids.

Administration of pyrene-linked fatty acids and lipids to cultured cells or an enveloped (vesicular stomatitis) virus induced photosensitization which, following irradiation with a long ultra-violet light (LUV), resulted in killing of the cells and loss of the infectivity of the virus with the following specific effects. (i) LUV illumination of the pyrene-sphingomyelin administered cultured skin fibroblasts derived from normal individuals and patients with Niemann-Pick disease permitted selective killing of the latter. (ii) Similarly LUV illumination of pyrenedodecanoic acid (P12) incubates of leukemic cell lines mixed with human bone marrow cells permitted selective killing of the former. (iii) LUV illumination of P12 incubates of vesicular stomatitis virus decreased the infectivity of the virus by up to 12 logs.

Phosphatidylcholine stimulates the activity of UDP-Gal beta 1-4 galactosyltransferase in normal human kidney proximal tumour cells.

Effects of various lipid components of low density lipoproteins (LDL) and serine on the regulation of UDP-Gal-beta 1-4-galactosyltransferase (GalT-2) activity have been investigated in normal proximal tubular (PT) cells. Addition of exogenous serine (0.1-0.75 mM), cholesterol (0-200 micrograms/ml medium), linoleic acid and oleic acid (0.1-0.75 mM) for 4 hr at 37 degrees C did not suppress the activity of GalT-2 in PT cells. Similarly, incubation of cells with glucosylceramide and lactosylceramide (25-50 micrograms/ml medium) did not alter GalT-2 activity in cells as compared to control. In contrast, palmitic acid (0-0.75 mM), phosphatidylethanolamine and sphingomyelin (0-200 micrograms/ml) stimulated GalT-2 activity by 20-36% as compared to control. Incubation of PT cells with D-alpha-dipalmitoyl phosphatidylcholine (0-200 micrograms/ml medium) also stimulated the activity of GalT-2, maximum stimulation (200%) occurring with 25 micrograms phosphatidylcholine/ml medium. However, at a higher concentration (200 micrograms/ml), the stimulation of the activity of GalT-2 was in the order of 27% compared to control. Dioleylphosphatidylcholine did not alter GalT-2 activity in PT cells. Thus, it is concluded that (i) various lipid components, sphingosine and serine present in LDL are not involved in the LDL-mediated suppression of GalT-2 activity in normal PT cells, and (ii) stringent structural requirements in the phosphatidylcholine molecule are necessary to exert a time and concentration dependent stimulation of GalT-2 activity.