title: Soyasaponins prevent H₂O₂-induced inhibition of gap junctional intercellular communication by scavenging reactive oxygen species in rat liver cells.
abstract: It appears to be more practical and effective to prevent carcinogenesis by targeting the tumor promotion stage. Gap junctional intercellular communication (GJIC) is strongly involved in carcinogenesis, especially the tumor promotion stage. Considerable interest has been focused on the chemoprevention activities of soyasaponin (SS), which are major phytochemicals found in soybeans and soy products. However, less is known about the preventive effects of SS (especially SS with different chemical structures) against tumor promoter-induced inhibition of GJIC. We investigated the protective effects of SS-A1, SS-A2, and SS-I against hydrogen peroxide (H2O2)-induced GJIC inhibition and reactive oxygen species (ROS) production in Buffalo rat liver (BRL) cells. The present results clearly show for the first time that SS-A1, SS-A2, and SS-I prevent the H2O2-induced GJIC inhibition by scavenging ROS in BRL cells in a dose-dependent manner at the concentration range of from 25 to 100 μg/mL. Soyasaponins attenuated the H2O2-induced ROS through potentiating the activities of superoxide dismutase and glutathione peroxidase. This may be an important mechanism by which SS protects against tumor promotion. In addition, various chemical structures of SS appear to exhibit different protective abilities against GJIC inhibition. This may partly attribute to their differences in ROS-scavenging activities.
authors.affiliation: a Department of Nutrition and Food Hygiene, School of Public Health and Tropical Medicine , Southern Medical University , Guangzhou , P.R. China.
authors.forename: Jiading
authors.initials: J
authors.lastname: Chen
authors.forename: Suxia
authors.initials: S
authors.lastname: Sun
authors.forename: Dingsheng
authors.initials: D
authors.lastname: Zha
authors.forename: Jiguo
authors.initials: J
authors.lastname: Wu
authors.forename: Limei
authors.initials: L
authors.lastname: Mao
authors.forename: Hong
authors.initials: H
authors.lastname: Deng
authors.forename: Xinwei
authors.initials: X
authors.lastname: Chu
authors.forename: Haiji
authors.initials: H
authors.lastname: Luo
authors.forename: Longying
authors.initials: L
authors.lastname: Zha
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D002450:Cell Communication / Q000187:drug effects*; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D020552:Comet Assay; D004249:DNA Damage / Q000187:drug effects; D016166:Free Radical Scavengers / Q000494:pharmacology*; D017629:Gap Junctions / Q000187:drug effects* / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D022781:Hepatocytes / Q000187:drug effects* / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000009:adverse effects; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000166:cytology / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012503:Saponins / Q000494:pharmacology*; D013025:Glycine max / Q000737:chemistry; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D012503:Saponins; D008315:Malondialdehyde; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase