In ovo exposure to nonylphenol and bisphenol A resulted in dose-independent feminization of male gonads in Japanese quail (Coturnix japonica) embryos

Abstract

Sex reversal effects of nonylphenol and bisphenol A on the gonads in F(1) (AWE × WE) Japanese quail (Coturnix japonica) embryos were investigated using an in vivo screening model developed previously. The F(1) (AWE × WE) Japanese quail are a useful avian model because sex differentiation is confirmed by the plumage color before hatching, ruled by a criss-cross inheritance. The nonylphenol at 200, 2,000, 20,000, and 200,000 ng/egg and bisphenol A at 20, 200, 2,000, and 20,000 ng/egg were injected into the egg white just before incubation. At 16 d of incubation, embryos were subjected to a complete necropsy, and their gonads were both grossly observed and examined histopathologically and morphometrically. Grossly, genetic sex was confirmed because plumage color coincided completely with the external sex phenotype of the gonads in all embryos. Histopathologically, feminization of the male gonad, called ovotestis, developed in the left testis in all nonylphenol- and bisphenol A-treated groups. The incidence of the lesion in all treated groups was significantly higher than that in the control group, whereas there were no dose-dependent changes in the incidence and area of the ovotestis in both nonylphenol- and bisphenol A-treated groups. The present study revealed that nonylphenol and bisphenol A have a dose-independent potential of ovotestis induction in the Japanese quail embryo.

Methoxychlor exposure induces oxidative stress and affects mouse oocyte meiotic maturation

“…Many natural and synthetic substances in the environment interfere with the physiological functions of humans and animals. In particular, endocrine-disrupting chemicals (EDCs) (Colborn et al, 1993) have attracted much interest because of their industrial and domestic applications versus Abbreviations: DSB, DNA double-strand break; EDC, endocrine-disrupting chemicals; GVBD, germinal vesicle breakdown; MI/II, metaphase I/II; MXC, methoxychlor; ROS, reactive oxygen species; SAC, spindle assembly checkpoint ß 2016 WILEY PERIODICALS, INC. their potential risks to animal health (Yang et al, 2006;Schug et al, 2011); indeed, EDCs affect sexual behaviors (Gray et al, 1989), fertility (Fowler et al, 2012), feminization (Oshima et al, 2012;Tian et al, 2012), and development of reproductive organs (Eroschenko et al, 1995). Recent studies demonstrated that EDCs also impact human health (Ho et al, 2012;Chauhan and Grissom, 2013;Faniband et al, 2014), directly interfering with steroid hormone-receptor binding and/or impacting cell signaling pathways (Henley and Korach, 2010).…”

Comparing the effects of tetrabromobisphenol-A, bisphenol A, and their potential replacement alternatives, TBBPA-bis(2,3-dibromopropyl ether) and bisphenol S, on cell viability and messenger ribonucleic acid expression in chicken embryonic hepatocytes

“…Over 2.7 million tonnes of BPA are produced globally each year and it is 1 of the most potent environmental estrogens based on a number of in vitro test systems . Bisphenol A induced Müllerian duct malformations in female bird embryos and feminization of male gonads in Japanese quail . Based on the estrogenic effects observed in avian species, the detection of BPA in liver tissue (0.94 ng/g wet wt) of a high‐trophic level avian species, the common cormorant ( Phalacrocorax carbo ) , is of concern.…”

Immunohistochemical Localization of Estrogen Receptor in the Embryonic Gonad of Male Quail Embryo During Gonadal Differentiation

“…From our pervious study, we found that in ovo exposure of phytoestrogen to male quail embryo caused thickening of the cortex of the left male gonad . The character of having thick cortex in male quail embryonic gonad after exposure to exogenous estrogens is called "ovotestis" (Perrin et al, 1995;Berg et al, 2001;Oshima et al, 2012). It has been reported that a number of ER in germinal epithelial cells were increased by phytoestrogen (Anderson et al, 1999).…”