Windows of Susceptibility and Consequences of Early Life Exposures to 17β–estradiol on Medaka (Oryzias latipes) Reproductive Success

Abstract

Estrogens and estrogen mimics are commonly found in surface waters and are associated with deleterious effects in fish populations. Impaired fertility and fecundity in fish following chronic exposures to estrogens and estrogen mimics during critical windows in development are well documented. However, information regarding differential reproductive effects of exposure within defined developmental stages remains sparse. In this study, reproductive capacity was assessed in Japanese medaka (Oryzias latipes) after exposure to two concentrations of 17β-estradiol (E2β; 2 ng/L and 50 ng/L) during four distinct stages of development: gonad development, gonad differentiation, development of secondary sex characteristics (SSC) and gametogenesis. Exposure to E2β did not adversely impact survival, hatch success, growth, or genotypic ratios. In contrast, exposure to 50 ng/L E2β during SSC development altered phenotypic ratios and SSC. Exposure to both E2β treatments reduced reproductive capacity (fertility, fecundity) by 7.3-57.4% in adult medaka breeding pairs, with hindrance of SSC development resulting in the largest disruption in breeding capacity (51.6-57.4% decrease) in the high concentration. This study documents differential effects among four critical stages of development and provides insight into factors (window of exposure, exposure concentration and duration of exposure period) contributing to reproductive disruption in fish.

Use of 5-azacytidine in a proof-of-concept study to evaluate the impact of pre-natal and post-natal exposures, as well as within generation persistent DNA methylation changes in Daphnia

“…It has been well documented, mainly in mice and human, that environmental stressors can interfere with epigenetic programming that occur during embryogenesis and tissue differentiation (De Felici 2011 ; Nestor et al 2015 ; Seisenberger et al 2013 ). This creates an extremely sensitive window in an individual’s development where disruption in this process can lead to severe health effects (Lee Pow et al 2017 ; Perera and Herbstman 2011 ). Therefore, the magnitude of biological response can be dependent on whether an individual encountered the stressor before or after embryogenesis (Lee Pow et al 2017 ; Mersha et al 2015 ).…”

“…This creates an extremely sensitive window in an individual’s development where disruption in this process can lead to severe health effects (Lee Pow et al 2017 ; Perera and Herbstman 2011 ). Therefore, the magnitude of biological response can be dependent on whether an individual encountered the stressor before or after embryogenesis (Lee Pow et al 2017 ; Mersha et al 2015 ). However, most importantly, this can lead to delayed adverse effects later in the life of an individual, long after the initial stressor has been removed, a concept referred to developmental origin of adult disease (Dolinoy and Jirtle 2008 ; Bailey 2015 ).…”

Survival, Growth, and Development in the Early Stages of the Tropical Gar Atractosteus tropicus: Developmental Critical Windows and the Influence of Temperature, Salinity, and Oxygen Availability

“…Most studies investigating critical windows have targeted morphological and physiological characteristics, maturation, metabolism, etc. across the different animal taxa [12,13,[15][16][17].…”

A systematic review of the evaluation of endocrine-disrupting chemicals in the Japanese medaka (Oryzias latipes) fish

“…Frontiers in Toxicology frontiersin.org 03 Dasmahapatra et al 10.3389/ftox.2023.1272368 In vitro reporter gene assay (affinity) (Tohyama et al, 2015) i) esr1: EC50 = 1.31 × 10 −10 M ii) esr1: EC50 = 1.31 × 10 −10 M iii) esr2b: EC50 = 8.16 × 10 −11 M Nimrod and Benson (1998), Patyna et al (1999), Foran et al (2000), Koger et al (2000), Shioda and Wakabayashi (2000), Metcalfe et al (2001), Tabata et al (2001), Kang et al (2002a), Kashiwada et al (2002), Oshima et al (2003), Balch et al (2004b), Hall et al (2005), Zeng et al (2005), Balch and Metcalfe (2006), Hirai et al (2006), Zhang et al (2008d), Sun et al (2009), Jin et al (2011a), Kamata et al (2011), Hirakawa et al (2012), Lee et al (2012), Flynn et al (2013), Lei et al (2013), Green et al (2015), Tohyama et al (2015), Inagaki et al (2016, Lee et al (2017a), Lee Pow et al (2017) In vitro reporter gene assay: EC50 = 0.00088 µM (Medaka esr1 agonist assay); IC50 = 0.14 µM (medaka arβ antagonist assay (Onishi et al, 2021) Scholz and Gutzeit (2000), Metcalfe et al (2001), Foran et al (2002), Islinger et al (2002), Lee et al (2002), Seki et al (2002), Balch et al (2004a), Noza...…”