title: Effect of gestational exposure to nonylphenol on the development and fertility of mouse offspring.
abstract: Nonylphenol (NP), a kind of environmental chemical, is thought to imitate endogenous hormones, inhibit the actions of hormones, and induce reproductive abnormalities. A number of experimental animals, usually rats, have been used to evaluate the potential reproductive toxicity of NP. However, the findings of previous studies were contradictory in some cases. Therefore, we used ICR mice as a biomodel for in utero study of NP. After mating, 8- to 12-week-old females were assigned to four groups (n=8) for subcutaneous injections from day 5 to 20 of gestation. Group I animals received corn oil alone as a control, while the mice of groups II, III and IV received NP at concentrations of 1/1000, 1/100 and 1/10 of the LD(50), respectively. A dose-dependent decrease was observed in terminal body weights of males of the F1 generation; however, a very small negative effect was only found in the females of the NP1/10 group. No significant effect was found on the liver weights of both sexes. The weights of the testis and epididymis were slightly decreased in the NP1/10 group. The NP1/100 treatment increased ovary weight considerably. The uterus weight tended to be increased in the NP treatment groups; however, there were large variations. The gestational exposure of the groups had no significant effect on the rate of pregnancy (94.4-100%) and the number of fetuses per litter (13.6-14.3 males, 12.3-13.7 females) compared with the control group. However, the overall mortality of fetuses/embryos was increased considerably in the NP1/100 (male: 13.9%) and NP1/10 (female: 9.8%) groups. These results suggest that exposure to NP in utero possibly affects the body weight and some reproductive organ weights, but does not influence the potential fertility of the F1 generation.
authors.affiliation: Laboratory of Animal Reproduction, Faculty of Agricultural Science, Yamagata University, Tsuruoka, Japan. naonao@tds1.tr.yamagata-u.ac.jp
authors.forename: Naoko
authors.initials: N
authors.lastname: Kimura
authors.forename: Takashi
authors.initials: T
authors.lastname: Kimura
authors.forename: Mikiko
authors.initials: M
authors.lastname: Suzuki
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Totsukawa
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D052244:Endocrine Disruptors / Q000633:toxicity*; D005260:Female; D005298:Fertility / Q000187:drug effects* / Q000502:physiology; D005836:Genitalia, Female / Q000187:drug effects* / Q000254:growth & development; D005837:Genitalia, Male / Q000187:drug effects* / Q000254:growth & development; D008098:Litter Size / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000254:growth & development; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009929:Organ Size / Q000502:physiology; D010053:Ovary / Q000187:drug effects / Q000254:growth & development; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013737:Testis / Q000187:drug effects / Q000254:growth & development; D014599:Uterus / Q000187:drug effects / Q000254:growth & development
chemical_list: D052244:Endocrine Disruptors; D010636:Phenols; C025256:nonylphenol