Morphological effects of the catecholestrogens on cells of the seminiferous tubules of Sprague-Dawley rats

Abstract

Estradiol-17P (E,) and rhe two catecholestrogens 2-OHE, and 4-OHE2, when daily administered at low doses of 10-40 ng/rat, were cytotoxic to the seminiferous epithelium. The structural changes seen after seven days exposure included abnormal meiotic type I1 cells with uneven chromosome distribution, the formation of binucleated and multinucleated giant cells, of which many were sloughed into the lumina of the seminiferous tubules. The effect of the 4-OHE, metabolites were always more pronounced than that of 2-OHE, or E,. After 21 daily exposures, 4-OHE2 proved to be very toxic, the seminiferous tubules were markedly denuded and numerous giant cells were present in the lumina. The catecholestrogens also caused a significant lowering ( P < 0.02) of testosterone serum levels after eight days exposure. E, at 40 ng/rat/day had no effect on testosterone production. At these low doses the catecholestrogens did not affect gonadotropin release after eight days exposure. Our results indicate that the morphological lesions could not exclusively be attributed to testosterone withdrawal and that a direct effect on developing spermatids is also indicated.

A Survey of Naturally-Occurring Steroid Hormones in Raw Milk and the Associated Health Risks in Tangshan City, Hebei Province, China

“…Female rats exposed prenatally to testosterone have altered reproduction later in life and no nipple development (i.e., masculinized mammary morphology), suggesting that gestational exposure to testosterone severely inhibits the normal development of females, rendering them unable to nurse their offspring [ 10 ]. In the male rat, exposure to estradiol was reported to induce morphological lesions and spermatogenic arrest [ 11 ]. Besides, the continued and massive intake of estrone may enhance tissue deposition and lead to obesity [ 12 ].…”

Effect of tamoxifen treatment on the semen quality and fertility of the male rat

“…The exact mechanisms of this duality are not understood completely, but they may depend on the expression of specific cell estrogen receptor variants (17). Alternatively, tamoxifen is converted to biologically active metabolites in the liver, after oral treatment, some of which have been reported to have greater affinity for the estrogen receptors in vitro and thus have the potential to modulate the tamoxifen-induced effects in vivo by exerting synergistic or antagonistic effects (18)(19)(20).…”

Analysis of steroid hormones in shell eggs from layer breeds common to Taiwan by liquid chromatography–tandem mass spectrometry

“…For several years, the presence of regulated hormone residues in food that exceeds the maximum prescribed limits has been a concern for public health. Animal studies have reported adverse effects, such as altered reproductive development, due to prenatal sex steroid hormone exposure (Seegers, van Aswegen, Nieuwoudt, & Joubert, 1991). Additionally, hormones derived from animal products have endocrine-disrupting effects in humans (Nakajima et al, 2015); therefore, steroid hormones may have a function in multiple diseases, including cancer (Krieger, 2008;Nachman & Smith, 2015).…”