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

被引：11

作者：

Salimath, BP ^{[1
]}

Tabassum, A

Anupama, EG

Bindumalini

Preeti, GB

Salimath, PV

机构：

[1] Univ Mysore, Dept Biochem, Mysore 570006, Karnataka, India

[2] Cent Food Technol Res Inst, Dept Biochem & Nutr, Mysore 570013, Karnataka, India

来源：

NUTRITION RESEARCH | 1999年 / 19卷 / 04期

关键词：

butyric acid; EAT cells; apoptosis; ROS generation; angiogenesis; phosphatase;

D O I：

10.1016/S0271-5317(99)00024-X

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

We have shown that butyric acid (in vivo) 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 in situ) included a dose dependent inhibition of generation of Reactive Oxygen Species(ROS) 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. (C) 1999 Elsevier Science Inc.

引用

页码：589 / 600

页数：12