The effect of ganodermic acid S on human platelets

Incubation of gel-filtered human platelets in ganodermic acid S (lanosta-7,9(11), 24-trien-3 beta, 15 alpha-diacetoxy-26-oic acid) showed that uptake of the agent by platelets was a simple diffusion process. The agent caused platelet aggregation at concentrations above 20 microM. Above the threshold, the extent of cell aggregation was in a linear relationship to the agent concentration. Below the aggregation threshold, platelets showed neither the resynthesis of [32P] phosphatidylinositol 4,5-bisphosphate ([32P]PIP2) and [32P] phosphatidylinositol 4-phosphate ([32P]PIP) nor the accumulation of [32P] phosphatidic acid ([32P]PA). The results suggested that ganodermic acid S caused the activation of PIP2 hydrolysis. Scanning electron microscopy revealed that the morphology of platelets below the aggregation threshold appeared to be spiculate discoid shape. Above the threshold, the cells rounded up to spiculate irregular forms.