Impacts of molt-inhibiting organochlorine compounds on epidermal ecdysteroid signaling in the fiddler crab, Uca pugilator, in vitro.
Because of their chemical stability and lipophilicity, many organochlorine compounds (OCs) can readily accumulate in fatty tissues of crustaceans. Several OCs have been reported to inhibit crustacean molting. To determine whether the disruption of crustacean molting by these OCs involves interference with ecdysteroid signaling in the epidermis, the impacts of five molt-inhibiting OCs on the level of N-acetyl-beta-glucosaminidase (NAG, EC 3.2.1.30) mRNA in cultured epidermal tissues from the fiddler crab, Uca pugilator, were investigated using quantitative real-time PCR. The NAG mRNA was found to be inducible by 20-hydroxyecdysone (20-HE) in cultured epidermal tissues. The inducibility of NAG mRNA in cultured epidermal tissues by 20-HE is not only further direct evidence that epidermal expression of NAG gene in U. pugilator is controlled by the molting hormone but also validates the use of the NAG mRNA as a biomarker for epidermal ecdysteroid signaling. When Aroclor 1242, 2,4,5-trichlorobiphenyl (PCB29), endosulfan or kepone was administered alone, the expression of NAG gene in cultured epidermal tissues was upregulated, while heptachlor had no effects. Under binary exposure to both 20-HE and an OC, a condition similar to the natural hormonal milieu of epidermal tissues of animals impacted by OCs, both Aroclor 1242 and endosulfan were found to be capable of antagonizing ecdysteroid signaling in cultured epidermal tissues. This antagonizing effect on epidermal ecdysteroid signaling can at least partly explain the inhibitory effects of these two agents on crustacean molting. PCB29, when given together with 20-HE, produced an additive effect on epidermal ecdysteroid signaling but such an additive effect was not observed when kepone was combined with 20-HE.
Meng
Yanling
Y
Department of Biological Sciences, Nicholls State University, Thibodaux, LA 70310, USA.
Zou
Enmin
E
D000118:Acetylglucosaminidase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001140:Aroclors / Q000494:pharmacology; D015415:Biomarkers / Q000378:metabolism; D003386:Brachyura / Q000187:drug effects*; D002478:Cells, Cultured; D007631:Chlordecone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D026461:Ecdysteroids / Q000378:metabolism*; D052244:Endocrine Disruptors / Q000494:pharmacology; D004726:Endosulfan / Q000494:pharmacology; D000078404:Epidermal Cells; D004817:Epidermis / Q000187:drug effects; D005260:Female; D006533:Heptachlor / Q000494:pharmacology; D006843:Hydrocarbons, Chlorinated / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D018978:Molting / Q000187:drug effects* / Q000235:genetics; D009994:Osmolar Concentration; D011078:Polychlorinated Biphenyls / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D015398:Signal Transduction / Q000187:drug effects*; D046509:Tissue Culture Techniques; D015854:Up-Regulation
D001140:Aroclors; D015415:Biomarkers; D026461:Ecdysteroids; D052244:Endocrine Disruptors; D006843:Hydrocarbons, Chlorinated; D012333:RNA, Messenger; C015550:2,4',5-trichlorobiphenyl; C027423:aroclor 1242; D006533:Heptachlor; D011078:Polychlorinated Biphenyls; D000118:Acetylglucosaminidase; D004726:Endosulfan; D007631:Chlordecone