title: Effects of transovarian exposure to p,p'-DDT and p,p'-DDE on avian reproduction using Japanese quails.
abstract: In the 1950s to 1970s developed countries reported declines in populations of raptorial and fish-eating birds and dichlorodiphenyltrichloroethane (DDT) and its metabolites were considered causative substances because they accumulated significantly in the tissues of wild birds and animals. However, except for the estrogenic effects of o,p'-DDT, a minor component of commercial DDT, there has been no compelling evidence that DDT directly affects avian reproductive systems. To assess the possible impact of DDT on development and reproduction of birds, exposure experiments to the major component of commercial DDT, p,p'-DDT, and its persistent metabolite, p,p'-dichlorodiphenyldichloroethylene (DDE), were performed using Japanese quail (Coturnix japonica) eggs; the test substances (3 to 100 μg/g) were injected into the yolk prior to incubation, and hatched chicks were raised to adulthood. p,p'-DDT had no significant effects on the morphology and function of the reproductive systems, although the hatchability of treated eggs was reduced at the highest dose (100 μg/g). High doses of p,p'-DDE slightly enhanced the eggshell forming ability of female quails; eggshell mass and thickness were increased at 30 μg/g or more although no morphological changes were observed in the oviduct. Transcriptions of the CYP11A1 gene in the ovaries, and of AHR and ARNT in the livers, of adult females were significantly increased at 3 μg/g or more of p,p'-DDT. Except for low hatchability, transovarian exposure to p,p'-DDT or p,p'-DDE did not markedly impair the avian reproductive systems, but the hormonal actions of these compounds are likely to change reproductive and hepatic functions even after maturation.
authors.affiliation: Research Center for Environmental Risk, National Institute for Environmental Studies.
authors.forename: Ryo
authors.initials: R
authors.lastname: Kamata
authors.forename: Fujio
authors.initials: F
authors.lastname: Shiraishi
authors.forename: Shinji
authors.initials: S
authors.lastname: Takahashi
authors.forename: Akira
authors.initials: A
authors.lastname: Shimizu
authors.forename: Daisuke
authors.initials: D
authors.lastname: Nakajima
authors.forename: Shiho
authors.initials: S
authors.lastname: Kageyama
authors.forename: Takushi
authors.initials: T
authors.lastname: Sasaki
authors.forename: Kyosuke
authors.initials: K
authors.lastname: Temma
mesh_terms: D000818:Animals; D051784:Aryl Hydrocarbon Receptor Nuclear Translocator / Q000378:metabolism; D002786:Cholesterol Side-Chain Cleavage Enzyme / Q000235:genetics; D003370:Coturnix / Q000502:physiology*; D003634:DDT / Q000009:adverse effects*; D003633:Dichlorodiphenyl Dichloroethylene / Q000009:adverse effects*; D004305:Dose-Response Relationship, Drug; D004625:Embryo, Nonmammalian / Q000187:drug effects* / Q000502:physiology; D047108:Embryonic Development / Q000187:drug effects; D005260:Female; D008099:Liver / Q000378:metabolism; D010053:Ovary / Q000201:enzymology; D010057:Oviducts / Q000187:drug effects; D010063:Ovum / Q000187:drug effects* / Q000502:physiology; D018336:Receptors, Aryl Hydrocarbon / Q000378:metabolism; D012098:Reproduction / Q000187:drug effects*; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D018336:Receptors, Aryl Hydrocarbon; D051784:Aryl Hydrocarbon Receptor Nuclear Translocator; D003633:Dichlorodiphenyl Dichloroethylene; D003634:DDT; C016340:o,p'-DDT; D002786:Cholesterol Side-Chain Cleavage Enzyme