Estrogen and Spermatogenesis

O’Donnell, Liza

doi:10.1016/b0-12-341103-3/00087-5

Cited by 155 publications

(245 citation statements)

References 13 publications

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“…However, it is not at all clear at this stage as to how estrogen mediates direct adverse effects within the testis. Estradiol treatment in male induces hormonal alterations affecting hypothalmo-pituitary-axis, but the role of estrogen arresting germ cell growth in the seminiferous epithelium has not been worked out in detail [16]. The aim of the present study was to investigate various patho-physiological processes triggered as a result of estradiol administration and their impact on germ cell status and survival in the seminiferous epithelium.…”

Section: Introductionmentioning

confidence: 98%

Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

et al. 2006

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In order to understand the pathogenesis of estradiol induced effects in the seminiferous epithelium, studies were undertaken in adult rats with estradiol-3-benzoate administered for different durations. After 30 d of treatment, a significant rise in lipid peroxidation with concomitant fall in the activities of superoxide dismutase and catalase was observed. Both, serum and intra-testicular testosterone levels were found severely depleted. Seminiferous epithelium was devoid of elongated spermatids and spermatozoa by 30 d of treatment. Number of spermatocytes and round spermatids were significantly (p < 0.001) reduced. Flowcytometric analysis confirmed a drastic reduction of the haploid cell population (1c peak). Beginning from day 10 of treatment, there was a consistent rise in the number of pyknotic/apoptotic germ cells in the seminiferous epithelium. A gradual increase in Bax protein expression was observed with the duration of treatment. The shift in Bax immunostaining from the cytoplasm and nucleus of germ cells (at 10 d of treatment) to only nuclei of cells by 30 d of treatment was also noticed. By this time testicular tissue showed three-fold increase in caspase-8 enzyme activity. Viable testicular cells isolated in vitro decreased drastically subsequent to different periods of estradiol treatment. The above findings substantiate the fact that the testicular pathogenesis of estradiol benzoate treatment may be primarily because of altered reproductive hormone levels and high oxidative stress leading to germ cell apoptosis and subsequent germ cell loss in the seminiferous epithelium.

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Section: Introductionmentioning

confidence: 98%

Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

et al. 2006

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“…et al, , 2005. In view of recent studies concerning the role of estrogen and phytoestrogen in both male and female reproduction (Simpson et al, 2000;O'Donnell et al, 2001;Robertson et al, 2002;Aquila et al, 2004;Tsai et al, 2005), the estrogenic activity of maca must be taken into consideration for evaluation of the in vivo activity of maca on fertility, potency, and growth rate as reported in the literature and in traditional medicine.…”

Section: Discussionmentioning

confidence: 98%

The in vitro biological activity of Lepidium meyenii extracts

et al. 2006

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The biological activity of methanolic and aqueous extracts from dehydrated hypocotyls of Lepidium meyenii (Brassicaceae, vernacular name "maca"), was studied on rat hepatocytes and human breast cancer MCF-7 cells. The extracts did not exhibit cytotoxicity in hepatocyte primary cultures up to 10 mg/ml as measured by the MTT viability test, and lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) leakage. Moreover, after 72 h, extracts inhibited LDH and AST leakage from the hepatocytes. When hepatocytes were intoxicated by t-butyl hydroperoxide, neither extract prevented oxidative damage. Both extracts showed weak antioxidant activity in the DPPH radical scavenging test with IC(50) values of 3.46 +/- 0.16 and 0.71 +/- 0.10 mg/ml, for aqueous and methanolic extracts, respectively. Thus, the observed effect on spontaneous enzyme leakage is probably mediated through mechanisms other than antioxidant activity. Both methanolic and aqueous extracts have shown estrogenic activity comparable with that of silymarin in MCF-7 cell line. Maca estrogenicity was exhibited in the range from 100 to 200 mug of extract per ml. The findings in the present study show that maca does not display in vitro hepatotoxicity. In contrast, a slight cytoprotective effect, probably not mediated by antioxidant capacity, was noted. Maca extracts exhibited estrogenic activity comparably to the effect of silymarin in MCF-7 cells.

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“…CYP19A1 expression has been observed in different stages of germ cell development (pachytene spermatocytes; round, elongating and elongated spermatids; and spermatozoa), in all somatic cells within the adult testis, and in spermatozoa in the mammalian epididymis [30,31]. Based on these Oestrogen action and male fertility: experimental and clinical findings reports, one could speculate that stem-like cell types, such as peritubular and spermatogonia, may programme their own protective mechanism against the deleterious effects of oestrogen action and thereby support the self-renewal of interstitial and germ cells.…”

Section: Aromatase Expression In Testismentioning

confidence: 99%

“…Compared with nuclear ERs, its binding affinity for 17b-oestradiol is considerably lower, and the association and dissociation rates are very rapid, on the order of minutes. The specificity of GPER for oestrogens is emphasized by the fact that other steroid hormones possess very low binding affinities for this receptor [30,55,56].…”

Section: Era and Erb And Their Isoformsmentioning

confidence: 99%

Oestrogen action and male fertility: experimental and clinical findings

Jia

et al. 2015

Cell. Mol. Life Sci.

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A proper balance between androgen and oestrogen is fundamental for normal male reproductive development and function in both animals and humans. This balance is governed by the cytochrome P450 aromatase, which is expressed also under spatio-temporal control. Oestrogen receptors ERα and/or ERβ, together with the membrane-associated G-protein-coupled functional ER (GPER), mediate the effects of oestrogen in the testis. Oestrogen action in male reproduction is more complex than previously predicted. The androgen/oestrogen balance and its regulation in the masculinisation programming window (MPW) during foetal life is the most critical period for the development of the male reproductive system. If this balance is impaired during the MPW, the male reproductive system may be negatively affected. Recent data from genetically modified mice and human infertile patients have shown that oestrogens may promote the engulfment of live Leydig cells by macrophages leading to male infertility. We also discuss recent data on environmental oestrogen exposure in men and rodents, where a rodent-human distinction is crucial and analyse some aspects of male fertility potentially related to impaired oestrogen/androgen balance.

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Estrogen and Spermatogenesis

Cited by 155 publications

References 13 publications

Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

The in vitro biological activity of Lepidium meyenii extracts

Oestrogen action and male fertility: experimental and clinical findings

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