title: Molokhia (Corchorus olitorius L.) extract suppresses transformation of the aryl hydrocarbon receptor induced by dioxins.
abstract: Dioxins enter the body mainly through diet and cause the various toxicological effects by binding to the cytosolic aryl hydrocarbon receptor (AhR) followed by its transformation. In recent reports, it has been shown that certain natural compounds suppress AhR transformation in vitro. In this study, we demonstrated that ethanolic extract from molokhia, known as Egyptian spinach, showed the strongest suppressive effect on AhR transformation induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in cell-free system using rat hepatic cytosol among 41 kinds of extracts from vegetables and fruits. The molokhia extract also suppressed TCDD-induced AhR transformation in mouse hepatoma Hepa-1c1c7 cells and in intestinal permeability system constructed with human colon adenocarcinoma Caco-2 cells and human hepatoma HepG2 cells. Moreover, oral administration of the molokhia extract (100mg/kg body weight) decreased 3-methylcholanthrene-induced AhR transformation to the control level by inhibiting translocation of the AhR from cytosol into the nucleus in the liver of rats. The molokhia extract-administered rat liver showed a tolerance to TCDD-induced AhR transformation by ex vivo experiment. These results indicate that molokhia is an attractive food for isolation and identification of a natural antagonist for the AhR.
authors.affiliation: Department of Biofunctional Chemistry, Faculty of Agriculture, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo 657-8501, Japan.
authors.forename: Shin
authors.initials: S
authors.lastname: Nishiumi
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Yabushita
authors.forename: Itsuko
authors.initials: I
authors.lastname: Fukuda
authors.forename: Rie
authors.initials: R
authors.lastname: Mukai
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Yoshida
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ashida
mesh_terms: D000818:Animals; D015153:Blotting, Western; D045744:Cell Line, Tumor; D019070:Cell Lineage / Q000187:drug effects; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D002474:Cell-Free System; D032381:Corchorus / Q000737:chemistry*; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D004147:Dioxins / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D004797:Enzyme-Linked Immunosorbent Assay; D000431:Ethanol; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D010539:Permeability; D010936:Plant Extracts / Q000494:pharmacology; D000072317:Polychlorinated Dibenzodioxins / Q000037:antagonists & inhibitors / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018336:Receptors, Aryl Hydrocarbon / Q000187:drug effects / Q000378:metabolism*; D012997:Solvents; D013723:Teratogens / Q000494:pharmacology; D014170:Transformation, Genetic / Q000187:drug effects*
chemical_list: D004147:Dioxins; D010936:Plant Extracts; D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon; D012997:Solvents; D013723:Teratogens; D000431:Ethanol; D019363:Cytochrome P-450 CYP1A1