z-logo
Premium
Blocking of intracellular ROS production by phytoglycoprotein (30 kDa) causes anti‐proliferation in bisphenol A‐stimulated Chang liver cells
Author(s) -
Oh PhilSun,
Lim KyeTaek
Publication year - 2008
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1334
Subject(s) - reactive oxygen species , cell growth , biochemistry , chemistry , protein kinase a , catalase , mapk/erk pathway , intracellular , microbiology and biotechnology , kinase , biology , antioxidant
Dioscorea batatas Decne (DBD) is traditionally used to heal inflammatory disease as a folk medicine. It was reported that a glycoprotein (DBD glycoprotein) with a molecular weight of 30 kDa was isolated from DBD and consists of carbohydrate (83.75%) and protein (16.25%) moieties. The previous results showed that it has a strong scavenging activity against hydroxyl radicals without any pro‐oxidant activity in the cell‐free system. The purpose of the present study was to show whether or not the DBD glycoprotein inhibits cell proliferation‐related signal transduction stimulated by bisphenol A (BPA, an environmental hormone) in Chang liver cells. The results in this study indicated that DBD glycoprotein (200 µg ml −1 ) has suppressive effects on abnormal cell viability, production of intracellular reactive oxygen species (ROS) and nitric oxide (NO) in BPA (50 µ m )‐induced Chang liver cells by blocking the phosphorylation of mitogen‐activated protein kinase (MAPK) and activating protein‐1 (AP‐1) activity. In addition, DBD glycoprotein (200 µg ml −1 ) normalized the activity of catalase (CAT) and glutathione peroxidase (GPx). Consequently, DBD glycoprotein inhibits the expression of proliferating cell nuclear antigen (PCNA, cell proliferation maker) stimulated by BPA. Therefore, it is speculated that DBD glycoprotein protects against carcinogenic events caused by BPA in Chang liver cells. Copyright © 2008 John Wiley & Sons, Ltd.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here