Category ZO L31 Exposure to low-dose bisphenol A causes hatching delays in

Medeka fish

Abstract Bisphenol A (BPA), a widely used monomer of polycarbonate plastics, has

raised concern as it has been found to leach out of the epoxy resin in

canned goods and common plastic containers such as baby bottles, and

water bottles (Whitteelsey, 2003). Bisphenol A is an estrogen mimic that

can act as an endocrine disruptor, which can interfere with hormone-

controlled physiological processes such as homeostasis, growth,

development, and reproduction (Howdeshell et al. 2003). With bisphenol A

leaching into so many common food and beverage containers, several

studies on fish and mice have shown that exposure to low doses of BPA

during embryo development hinder the development of the embryo, and

may cause adverse reproductive affects (Ramakrishnan and Wayne,

2008). In this study, Japanese Medaka (Oryzias latipes) fish embryos at

both 5 hours post-fertilization and 4 days post-fertilization were exposed

to varying levels of bisphenol A: 0 μg/L, 200 μg/L, and 1,000

μg/L. The Medaka embryos exposed to BPA at both 5 hours post-

fertilization and 4 days post-fertilization had a delayed hatch rates

compared to the age related controls. Thus, the results showed that

bisphenol A exposure in Medaka embryos decelerated rate of hatch. In

previous studies examining the biological reasons for BPA disrupting the

normal hatching behavior, it has been concluded that BPA disorders the

osmoregulation, the maintenance of an optimal constant osmotic pressure

in the body of a living organism, and thereby affects the normal hatching

behavior and the morphogenesis, the development of structural features

(Zhou et at., 2010). Moreover, as well as affecting the osmoregulation of

the embryos, other studies of the effects of BPA in fish embryonic

development have speculated that the BPA interferes with the normal

function of endogenous hormones, and affects the cell cycle by causing a

delay in the metaphase stage of mitosis by destabilizing microtubules

(Zhou et al., 2010). Altogether, the embryos exposed to 200 μg/L

and 1,000 μg/L of BPA four days after fertilization and the embryos

exposed to 200 μg/L of BPA five hours after fertilization had a

decreased rate of hatch because bisphenol A affected the physiological

equilibrium of the embryos and caused the eggs to lose control of the cell-

cycle regulation (Zhou et al., 2010).

Bibliography Howdeshell KL, Peterman PH, Judy BM, Taylor JA, Orazio CE, Ruhlen RL,

Saal FS, Welshons WV. 2003. Bisphenol A Is Released from Used

Polycarbonate Cages into Water at Room Temperature. Envirmental Health

Perspectives 9:1180-7.



Ramakrishnan S, Wayne NL. 2008. Impact of bisphenol A on early

embryonic development and reproductive maturation. Reproductive

Toxicology 2:177-183.



Whitteelsey FC. 2003. Hazards of Hydration. Sierra 6: 16-18.



Zhou J, Zhu XS, Cai ZH. 2010. The impacts of bisphenol A (BPA) on

abalone (Haliotis disersicolor supertexta) embryonic development.

Chemosphere 56: 459-510.
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