title: Effect of 4-nonylphenol on cell proliferation and adipocyte formation in cultures of fully differentiated 3T3-L1 cells.
abstract: The effect of 4-nonylphenol (NP) on cell proliferation and adipocyte formation was examined in cultures of fully differentiated 3T3-L1 cells. Following the hormonal induction of differentiation into adipocytes, 3T3-L1 cells were treated for 8 days with or without NP. NP at 5 and 10 microg/ml increased the DNA content by 32% and 68%, respectively, compared with that of the untreated cultures, in which NP was absent during the treatment period. There were many more bromodeoxyuridine (BrdU)-positive cells in the NP-treated cultures, in which NP was present at a concentration of 10 microg/ml during the treatment period, compared to the untreated cultures. These results indicate that NP had the ability to stimulate the proliferation of fully differentiated 3T3-L1 cells. NP at 5 and 10 microg/ml decreased the triacylglycerol (TG) content by 26% and 58%, respectively, and decreased the lipoprotein lipase (LPL) activity by 51% and 71%, respectively. The lipid droplets in individual cells of the NP-treated cultures were smaller than those of the untreated cultures. The mRNA levels of LPL and adipocyte-specific fatty acid binding protein (aP2) were considerably lower in the NP-treated cultures than in the untreated cultures. Thus, NP also had the ability to inhibit adipocyte formation in cultures of fully differentiated 3T3-L1 cells. A study using an antiestrogen ICI 182,780 showed that the NP-stimulated cell proliferation was mediated partly by the estrogen receptor, while the NP-induced inhibition of adipocyte formation was mediated by a mechanism other than the estrogen receptor.
authors.affiliation: Department of Medical Laboratory Technology, Ehime College of Health Science, Takooda, Tobe-cho, Iyo-gun, Ehime 791-2101, Japan. hmasuno@ehime-chs.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Masuno
authors.forename: Shoko
authors.initials: S
authors.lastname: Okamoto
authors.forename: Jun
authors.initials: J
authors.lastname: Iwanami
authors.forename: Katsuhisa
authors.initials: K
authors.lastname: Honda
authors.forename: Takahiko
authors.initials: T
authors.lastname: Shiosaka
authors.forename: Teruki
authors.initials: T
authors.lastname: Kidani
authors.forename: Kenshi
authors.initials: K
authors.lastname: Sakayama
authors.forename: Haruyasu
authors.initials: H
authors.lastname: Yamamoto
mesh_terms: D041721:3T3-L1 Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D015152:Blotting, Northern; D001973:Bromodeoxyuridine / Q000378:metabolism; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics; D002452:Cell Count; D002454:Cell Differentiation / Q000187:drug effects*; D002455:Cell Division / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000031:analogs & derivatives* / Q000494:pharmacology; D020847:Estrogen Receptor Modulators / Q000494:pharmacology; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D000077267:Fulvestrant; D008071:Lipoprotein Lipase / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D009419:Nerve Tissue Proteins; D010636:Phenols / Q000633:toxicity*; D012333:RNA, Messenger / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D020847:Estrogen Receptor Modulators; C086936:Fabp7 protein, mouse; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D009419:Nerve Tissue Proteins; D010636:Phenols; D012333:RNA, Messenger; D014280:Triglycerides; D000077267:Fulvestrant; D004958:Estradiol; D008071:Lipoprotein Lipase; D001973:Bromodeoxyuridine; C041594:4-nonylphenol