Histologic study of testis injury after bisphenol A exposure in mice

Abstract

The health effects of bisphenol A (BPA) have become a great concern in recent years. In this study, the reproductive toxicity of BPA was investigated. Male CD-1 mice were orally administrated with BPA (0, 100, 300 and 600 mg kg body weight) for 56 consecutive days. Results showed that relative testis weight to total body weight was significantly lower in the high-dose group ( p < 0.01, p < 0.05). Microscopic examination under light and transmission electron microscopes showed disorders of spermatogenesis after BPA exposure, including rough basal lamina of seminiferous tubules and damage of tight junctions between Sertoli cells. Further study by terminal-deoxynucleoitidyl transferase-mediated nick end labelling assay showed a significant induction of apoptosis in the testis tissue of the BPA groups ( p < 0.01). Immunohistochemical study found that the expression of androgen-binding protein (ABP) was significantly decreased in BPA-treated mice ( p < 0.01). Our results indicated that impairment of the basal lamina of seminiferous tubules and tight junctions may contribute to BPA-induced cell injury. A decrease in the level of ABP could be the possible mechanism for the reproductive toxicity of BPA. These findings provided direct evidence and novel insight into the reproductive toxicity of BPA and may have implications for understanding the toxicity of other endocrine disruptors.

The possible protective effect of Omega 3 fatty acids against Bisphenol A induced disruption of pituitary-testicular axis in albino rat. Biohemical, Histological and Immunohistochemical study

“…It is reported that a decrease in the level testosterone in BPA-treated rats led to atrophy of seminiferous tubules, degeneration of cells, and complete absence of spermatogenesis [21] . Also, the impairment of the basal lamina of seminiferous tubules and damaged tight junctions between sertoli cells could be attributed to BPA-induced cell injury as reported by [22] . Additionally, the intercellular spaces represent progressive degenerative changes affecting cell membrane integrity secondary to oxidative stress induced by BPA.…”

“…BPA may act via several different mechanisms involving interaction with estrogen receptors and/or by production of a minor but potent estrogenic metabolite [30] . A decrease in the level of androgen binding protein could be the possible mechanism for the reproductive toxicity of BPA [22] . Others reported that a low BPA concentration can induce spermatogenesis disorders mainly through decreasing androgen receptor expression [26] .…”

Effects of bisphenol A exposure on DNA integrity and protamination of mouse spermatozoa

“…Small fragments (1 mm 3 ) of dissected testes were removed and fixed in 2.5% glutaraldehyde in 0.1 M phosphate buffer (pH 7.4), post-fixed in 1% OsO 4 . The following protocol referred to the standard procedures (Tian et al, 2017). The ultrastructural features of testicular sections were examined under a transmission electron microscope (TEM) (Hitachi, HT7700, Japan).…”

Bisphenols as a Legacy Pollutant, and Their Effects on Organ Vulnerability

“…Numerous studies in animal models have reported the deleterious effects of exposure to bisphenols. Tian et al found that male CD-1 mice exposed to BPA had decreased testis weight, damage to basal lamina of seminiferous tubules and tight junctions between Sertoli cells, and decreased levels of the androgen-binding protein [61]. BPA exposure of pregnant CD-1 mice results in altering the tissue organization of ovaries and mammary glands, and alters the estrous cycle in adulthood via modulation of their morphogenesis specific genes' expression [62].…”