Bisphenol-A (BPA), a plastic compound used in dental sealants and to coat food and drink containers, has been in the news lately, in large part because of concerns over its effects as an endocrine disruptor. Specifically, BPA is thought to cause feminization of male mammals, including humans, through its ability to mimic estrogens and interact with estrogen receptors. Of course, sex hormones are crucial for reproductive development and differentiation in other vertebrates, and in 2002, Furuya and colleagues examined the effects of BPA exposure on the growth of combs and testes in male White Leghorn chickens. The researchers fed BPA, dissolved in corn oil, to male chicks each week, starting at age two weeks, and then examined the weight of combs, and the differentiation of testes, in these birds at age 16 weeks. Although both control and BPA-exposed chicks had similar body weights at the end of the study period, comb development and testes differentiation were abnormal in those birds that had been fed bisphenol-A. Specifically, BPA exposure reduced the size of seminiferous tubules in the testes, and resulted in a decrease in the number of spermatids and mature sperms.
BPA exposure reduces comb size (from Furuya et al., 2002)
This initial study was followed by more detailed investigations of the dose-dependent effects of BPA on male sexual differentiation in White Leghorn chickens (Furuya et al., 2005). The researchers point out in the introduction that both environmental levels of BPA, and differential effects of estrogens on avian testes differentiation (e.g. exposure of male chicken embryos to estrogens results in the development of ovarian tissue within the testes), must be considered in study design. Accordingly, the doses of BPA administered orally to the male chicks ranged from 2 micrograms per kilogram body weight, to 200 milligrams per kilogram body weight. In addition, Furuya and colleagues analyzed spermatogenesis in more detail, and examined estrogen receptor expression using RT-PCR.
BPA exposure reduces the number of spermatids, and the diameter of seminiferous tubules, in the testes of White Leghorn chickens (from Furuya et al., 2005)
All doses of BPA caused a decrease in the weights of the combs, wattles, and testes in experimental group birds, as compared to controls, when examined at 15, 20, and 25 weeks of age. Even low doses of BPA (20 micrograms) caused decreases in the diameters of seminiferous tubules, and reduced the numbers of spermatocytes, spermatids, and spermatogonia. From the results of their immunostaining experiments for proliferating cell nuclear antigen (PCNA), the investigators propose that BPA delays the onset of cell proliferation critical for normal spermatogenesis. Low doses of BPA also increased messenger RNA levels for the estrogen receptor alpha gene by 10 weeks, but differences were only apparent with the highest BPA dose (200 milligrams) by 25 weeks. Although a number of studies indicate that BPA at environmental levels may not significantly affect the development of the mammalian reproductive system, these results with post-hatching chickens suggest that male birds may be more sensitive to the feminizing effects of xenoestrogens.
Furuya, M., Sasaki, F., Hassanin, A.M.A., Kuwahara, S., and Tsukamoto, Y. (2002) Effects of bisphenol-A on the growth of comb and testes of male chicken. Canadian J. Veterinary Research 67, 68-71.
FURUYA, M., ADACHI, K., KUWAHARA, S., OGAWA, K., TSUKAMOTO, Y. (2006). Inhibition of male chick phenotypes and spermatogenesis by Bisphenol-A. Life Sciences, 78(15), 1767-1776. DOI: 10.1016/j.lfs.2005.08.016