Prehemolytic erythrocyte deformability changes caused by trichothecene T-2 toxin: an ektacytometer study.
The trichothecene mycotoxin, T-2, is responsible for a wide range of human diseases and animal toxicoses and is known to cause hemolysis of erythrocytes, over time. In order to determine the initial, prehemolytic effect of T-2 toxin on the red cell, we analysed the osmotic deformability pattern using the ektacytometer. After a lag period of 10-60 minutes, hemolysis of T-2 treated red cells is associated with a loss of deformability. During this lag phase there is echinocytosis but no hemolysis. Concurrent with production of echinocytosis there is an initial left shift of the osmotic deformability profile so that the points of maximum and minimum deformability occur in solutions of lower osmolality than normal. The elongation index is also increased. This pattern, one of increased surface area and/or reduced volume (cellular dehydration), represents the initial effect of T-2 toxin on the red cell and is transient. Very quickly, the deformability profile returns to normal, then shifts to the right with a subsequent decrease in elongation index as hemolysis ensues. These changes are independent of the presence of Ca++ and Mg++ and reduced cellular levels of ATP. The findings are consistent with T-2 toxin interacting directly with the cell membrane.
D000255:Adenosine Triphosphate / Q000032:analysis; D002118:Calcium / Q000494:pharmacology; D004907:Erythrocyte Deformability / Q000187:drug effects*; D004909:Erythrocyte Indices / Q000187:drug effects / Q000295:instrumentation; D004910:Erythrocyte Membrane / Q000187:drug effects; D005260:Female; D006461:Hemolysis / Q000187:drug effects; D006801:Humans; D008274:Magnesium / Q000494:pharmacology; D012717:Sesquiterpenes / Q000494:pharmacology*; D013605:T-2 Toxin / Q000494:pharmacology*
D012717:Sesquiterpenes; D000255:Adenosine Triphosphate; D008274:Magnesium; D013605:T-2 Toxin; D002118:Calcium