Changes in male genital organs of mice exposed neonatally to tamoxifen.

Iguchi, Taisen; Hirokawa, Mariko

doi:10.2183/pjab.62.157

Cited by 13 publications

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“…We therefore tested the effects of tamoxifen treatment because this compound displays a range of effects from complete antagonism to pure estrogen agonism, depending on the concentration, sex of the animal, target organ, and period of use (50). Neonatal treatment of male mice with tamoxifen induces various abnormalities to the reproductive tract (36,51), and its administration to adult male rats reduced the weight of the SV, ventral prostate, and epididymides (52,53). Although tamoxifen treatment was able to induce immunoexpression of PR and to slightly upregulate immunoexpression of ERα in stromal tissue of the SVs in the present studies, it had only minor effects on epithelial immunoexpression of AR and on the stromal:epithelial tissue ratio.…”

Section: Discussionmentioning

confidence: 99%

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Relationship between expression of sex steroid receptors and structure of the seminal vesicles after neonatal treatment of rats with potent or weak estrogens.

Williams

Fisher

Turner

et al. 2001

Environ Health Perspect

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In this study we evaluated the effect of manipulating the estrogen and androgen environment of the neonatal male rat on subsequent immunoexpression of sex steroid receptors in the seminal vesicles (SVs) at age 18 days. The aim was to establish to what extent such changes were associated with and predictive of changes in SV structure/composition. Treatments were either diethylstilbestrol (DES; 10, 1, or 0.1 microg/injection), ethinyl estradiol (EE; 10 microg/injection), tamoxifen (2 mg/kg/day), flutamide (50 mg/kg), a gonadotropin-releasing hormone antagonist (GnRHa; 10 mg/kg), genistein (4 mg/kg/day), octylphenol (2 mg/injection), or bisphenol A (0.5 mg/injection). Compared with controls, treatment with DES (10 microg) induced loss of epithelial and stromal androgen receptor (AR) immunoexpression coincident with induction of stromal progesterone receptor (PR) immunoexpression and upregulation of stromal immunoexpression of estrogen receptor-alpha (ERalpha). These changes were associated with gross distortion (increase) of the normal stromal:epithelial tissue proportions in the SVs. DES (1 microg) and EE induced similar but less pronounced changes, and DES (0.1 microg) had no noticeable effect. Tamoxifen and flutamide induced PR and slightly upregulated ERalpha immunoexpression but had only a minor or no effect on AR expression and the stromal:epithelial ratio, though flutamide retarded normal development of the SVs. The latter was also evident in GnRHa-treated males, but otherwise this treatment had no effect on AR and PR immunoexpression. None of the foregoing treatments had any detectable effect on the immunoexpression of ERss in stromal or epithelial cells. The major treatment-induced changes in immunoexpression of AR, PR, and ERalpha and lack of change in ERss were confirmed by Western blots of SV protein extracts. None of the three weak (environmental) estrogens tested caused any detectable change in sex steroid receptor immunoexpression or SV tissue composition. We conclude that treatment-induced loss of AR is a prerequisite for altered stromal:epithelial proportions in the SVs and that such loss is always associated with induction of PR and upregulation of ERalpha; the latter two changes are insufficient on their own to bring about such a change. Nevertheless, induction of PR expression was always associated with altered SV development and is a potentially useful marker because it is not normally expressed in male reproductive tissues.

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Section: Discussionmentioning

confidence: 99%

“…c) We administered the mixed estrogen agonist/antagonist tamoxifen (Sigma) at a dose of 2 mg/kg in 20 µL corn oil on days 2-16. This dose was chosen based on previous studies in the literature (36). d) We administered bisphenol A (BisA; Aldrich Chemicals Limited, Dorset UK) at a dose of 0.5 mg in 20 µL corn oil on days 2-12.…”

Section: Methodsmentioning

confidence: 99%

Relationship between expression of sex steroid receptors and structure of the seminal vesicles after neonatal treatment of rats with potent or weak estrogens.

Williams

Fisher

Turner

et al. 2001

Environ Health Perspect

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“…However, TAM treatment induced a severe decrease in sperm motility of caudal epididymides in this study. Iguchi et al (1986Iguchi et al ( , 1990) demonstrated that neonatal exposure to TAM caused a long-lasting suppression of spermatogenesis in mice, atrophy of testes. TAM treatment could lead to a reduction in sperm motion which is reponsible for onset of infertility before testicular lesion.…”

Section: Discussionmentioning

confidence: 99%

Reproductive Effects of Early Neonatal Exposure to Diethylstilbestrol or Tamoxifen in Rats

Kuwagata¹,

Saito²,

Yoshimura³

et al. 1999

Congenital Anomalies

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To evaluate the effects of potential estrogenic or anti‐estrogenic compounds on reproduction, male and female Sprague‐Dawley rats were injected subcutaneously with 50 μg/kg diethylstilbestrol (DES) or 20 mg/kg tamoxifen (TAM) from postnatal day 1 to 5. Growth, estrous cycle, locomotor activity, and reproductive function including masculine sexual behavior, sperm motion, and development of reproductive organs were examined. Decrease in body weight gain and abnormal estrous cycle, such as persistent estrous, or prolonged estrous cycle were observed following early neonatal exposure to DES or TAM, while there was no effect on locomotor activity evaluated in the open field in the DES‐or TAM‐treated group. A marked decrease in sperm motility was found in the TAM‐treated group. Anatomical and histological alterations of reproductive organs were observed in male and female rats in the DES‐treated group and in female rats in the TAM‐treated group. Early neonatal exposure to DES or TAM affected the masculine sexual behavior, resulting in a marked decrease in the ability to copulate and in fertility. In matings of the DES‐or TAM‐treated rats and intact rats, none of the treated females copulated successfully, whereas approximately 30% of treated males showed normal fertility. These results suggested that early neonatal exposure to DES or TAM induced more marked reproductive dysfunction after puberty in females than in males.

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“…En ratones macho, el Tx perjudica el desarrollo de los testículos y las glándulas accesorias después de la administración neonatal (24 horas postnacimiento; 20 o 100 μg/día durante cinco días; Iguchi, 1986), y genera infertilidad (Taguchi 1987). El Tx impide la interacción del estradiol con su receptor en el hipotálamo, además de inhibir la enzima aromatasa, lo que conduce a la feminización cerebral (Döhler et al 1985).…”

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A single neonatal administration of soybean oil and/or tamoxifen affects permanently the testis histomorphology in adult rats.

et al. 2016

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ResumenEl objetivo de este estudio fue evaluar el efecto de la administración de tamoxifeno (Tx) y aceite de soya (SO) durante el periodo crítico de la diferenciación sexual hipotalámica en ratas macho recién nacidas, en el contexto de la histomorfología gonadal durante la edad adulta. Los animales se dividieron al azar en tres grupos (n = 5 cada uno). Una hora después del nacimiento, un grupo fue tratado por vía subcutánea con 200 μg de Tx y 20 μL de SO comercial como vehículo; mientras otro grupo fue tratado solo con 20 μL de SO, y el grupo control no recibió ningún tratamiento. Todas las ratas se pesaron y sacrificaron por dislocación cervical a los 90 días postratamiento. Se extrajeron los testículos, se pesaron y procesaron para la evaluación histológica. La administración única de Tx y de SO durante el periodo crítico de la diferenciación sexual del hipotálamo altera de forma permanente la histomorfología testicular, la espermatogénesis y el peso corporal en la edad adulta. Las alteraciones incluyen: vacuolización, reducción del número de espermatogonias y de células de Sertoli. La administración de Tx redujo el peso testicular, el diámetro y el área de los túbulos seminíferos, así como la altura del epitelio germinal, e incrementó el espacio intertubular. El SO redujo el número de espermatocitos y espermátides, incluso más que el Tx. No se afectó el número de células de Leydig. La posibilidad de que el aceite de soya actúe como disruptor endócrino, amerita más atención y abre la posibilidad para el desarrollo de nuevos métodos de control de plagas.Palabras clave: disruptores endócrinos; tamoxifeno; aceite de soya; diferenciación sexual del hipotálamo; morfología testicular. IntroducciónDurante el desarrollo de la rata, en el periodo crítico de la diferenciación sexual a nivel cerebral, el cerebro de estos roedores macho está expuesto a altos niveles de testosterona de origen testicular, los cuales se incrementan a finales de la gestación, principalmente dos horas después del nacimiento (Anne et al. 2011). En las neuronas, la testosterona se convierte a estrógenos mediante la intervención Administración neonatal única de aceite de soya y/o tamoxifeno afecta permanentemente a la histomorfología testicular en ratas adultas

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Changes in male genital organs of mice exposed neonatally to tamoxifen.

Cited by 13 publications

References 0 publications

Relationship between expression of sex steroid receptors and structure of the seminal vesicles after neonatal treatment of rats with potent or weak estrogens.

Relationship between expression of sex steroid receptors and structure of the seminal vesicles after neonatal treatment of rats with potent or weak estrogens.

Reproductive Effects of Early Neonatal Exposure to Diethylstilbestrol or Tamoxifen in Rats

A single neonatal administration of soybean oil and/or tamoxifen affects permanently the testis histomorphology in adult rats.

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