Summary
The steroid saponins digitonin and saponin white, compounds effective in disrupting
membrane lipid-protein, have been shown to activate STA precursor.
Ultracentrifuge studies showed a radical alteration in the floatation behaviour of
the precursor complex on activation by digitonin, indicating an increase in its molecular
size.
Gel-filtration studies, on the other hand, revealed that activation by digitonin was
reversible, since passage down a Sephadex G-200 column not only removed digitonin
but abolished all activity, the latter being fully restored by the further addition
of digitonin. Furthermore, since the elution positions of inactive precursor and deactivated
STA were identical, this de-activation was accompanied by the return of the complex
to its original size. The failure of cardiac glycosides, other than digitonin, to
activate the precursor may be due to their being more hydrophobic and suggests that
hypercoagulability leading to possible thrombosis does not arise from their therapeutic
use.
