Molecular mechanism of action of butyric acid in Ehrlich ascites tumor cells.

We have shown that butyric acid (in viva) decreased
cell proliferation of Ehrlich Ascites Tumor (EAT)
cells. This effect of butyric acid is attributed
to induction of apoptosis in EAT cells, as
evidenced by prevalent apoptotic morphology in EAT
cells. Molecular effects of butyric acid (in vivo
and -i-n situ) included a dose dependent inhibition
of generation of Reactive Oxygen Species(R0.S) with
IC50 value of 5 uM. Butyric acid inhibited
neovascularization in the peritoneum of EAT
bearing mice. The absence of permeability factor(s)
in exudate of mice bearing EAT cells treated with
butyric acid, can either be due to inhibition of
secretion of growth factors or repression of their
expression by butyric acid. Further, butyric acid
not only activated a cytosolic phosphatase but also
induced its expression as evidenced by immunological
staining, using anti-phosphatase antibodies.