scholarly journals Atrazine affects the morphophysiology, tissue homeostasis and aromatase expression in the efferent ductules of adult rats with mild alterations in the ventral prostate

Chemosphere ◽  
2018 ◽  
Vol 193 ◽  
pp. 958-967 ◽  
Author(s):  
Elisângela Martins-Santos ◽  
Cristiano Guimarães Pimenta ◽  
Pollyana Rabelo Nunes Campos ◽  
André Gustavo Oliveira ◽  
Germán Arturo Bohórquez Mahecha ◽  
...  
Keyword(s):  
Tissue Homeostasis ◽  
Ventral Prostate ◽  
Adult Rats ◽  
Aromatase Expression ◽  
Efferent Ductules

Testicular serotonin is related to mast cells but not to Leydig cells in the rat

1995 ◽  
Vol 146 (1) ◽  
pp. 15-21 ◽  
Author(s):  
R Aguilar ◽  
F Antón ◽  
C Bellido ◽  
E Aguilar ◽  
F Gaytan
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Interstitial Fluid ◽  
Ventral Prostate ◽  
Adult Rats ◽  
Cell Numbers ◽  
Oestradiol Benzoate ◽  
Testicular Capsule

Abstract Testicular serotonin (5HT) concentrations were determined by HPLC in the testes of rats treated neonatally with oestradiol benzoate (EB) and in adult rats treated with the Leydig cell cytotoxic ethylene dimethane sulphonate (EDS). 5HT concentrations were related to mast cell numbers. EB-treated rats showed an accumulation of mast cells in the testes at 35 and 70 days of age and increased 5HT concentrations in both the interstitial fluid and the testicular capsule, whereas no increases in 5HT concentrations or in the number of mast cells were found for the ventral prostate of these animals. On the contrary, 5HT concentrations were not related to the number of Leydig cells. In EB-treated rats, in which Leydig cells were nearly absent at 35 days of age, 5HT concentrations were significantly increased. Furthermore, EDS-treated rats did not show significant changes in 5HT concentrations, in spite of the elimination of Leydig cells. These data suggest that mast cells are a major source of serotonin in the rat testis. Journal of Endocrinology (1995) 146, 15–21

INFLUENCE OF THE ADRENAL GLAND ON PROSTATIC ACTIVITY IN ADULT RATS

1973 ◽  
Vol 59 (2) ◽  
pp. 335-344 ◽  
Author(s):  
B. G. MOBBS ◽  
I. E. JOHNSON ◽  
J. G. CONNOLLY
Keyword(s):  
Nucleic Acid ◽  
Adrenal Gland ◽  
Acid Content ◽  
Prostate Gland ◽  
Ventral Prostate ◽  
Nucleic Acid Content ◽  
Adult Rats ◽  
Intact Control ◽  
Accessory Sex Glands ◽  
Target Organs

SUMMARY The weight of the accessory sex glands, and the citrate and nucleic acid content of the ventral prostate (VP) glands, were examined in animals which had been adrenalectomized 30 days previously and in intact control rats. Adrenalectomy greatly reduced the citrate content, but did not affect the nucleic acid content of the VP. It was concluded that the adrenals stimulated prostatic function rather than growth. The concentration of radioactivity in the accessory sex glands of adrenalectomized and/or castrated animals after the injection of [3H]testosterone was compared with that in sham-operated controls. Radioactivity was related to the DNA content of the VP of the four groups. It was concluded that adrenalectomy facilitated the uptake and/or retention of androgen. [3H]Corticosterone was not retained by any of the accessory sex glands of animals adrenalectomized and castrated 2 days previously. It seems unlikely that the glands should be considered 'target organs' for corticosterone in the accepted sense of the term, but it is suggested that corticosteroids may help to maintain the balance between differentiation and growth in the VP by influencing the metabolism of androgens by the prostate gland.

scholarly journals Letrozole effect in murine ventral prostate

2009 ◽  
Vol 1 (1) ◽  
pp. 45-53
Author(s):  
Manuel García ◽  
Hernandes Corralho
Keyword(s):  
Androgen Receptor ◽  
Prostate Gland ◽  
Serum Levels ◽  
Receptor Expression ◽  
Ventral Prostate ◽  
Proliferation Index ◽  
Basal Cells ◽  
Adult Rats ◽  
Hormone Levels ◽  
Letrozole Treatment

The prostate gland is regulated by steroid hormones and complex interactions based on a subtle balance between androgen and estrogen (E2) regulate prostatic development and physiology. Interestingly, the changes in steroid hormone levels at old ages affect the hormonal milieu and contribute to the evolution of the pathological changes of the gland. We have analyzed the effects of letrozole, an aromatase inhibitor, on the structure in the ventral prostate of control and castrated adult rats. The results demonstrated alterations in prostate physiology after letrozole treatment. Serum levels of testosterone, prostate weight and proliferative index in luminal and basal cells were increased. Estrogen serum levels were not altered dramatically, in contrast to slight increase in gonadotrophin hormones seen in the castrated animals. Castration did not alter the proliferation index of basal cells. Reorganization of tissue compartments was seen with significant increase in letrozole treated animals. A decrease in androgen receptor expression was seen 21-days after the beginning of treatment with letrozole. These results were confirmed by immunohistochemistry. These results reveal new aspects in the relationship between androgen receptor and steroid metabolism in the prostate gland, demonstrating that alteration in hormone levels during a short time period induces significant alterations in prostate homeostasis. 

305. Effects of moderate spinal cord injury on the expression of a barrier marker in endothelial cells of the testis and in the prostate of rats

2005 ◽  
Vol 17 (9) ◽  
pp. 130
Author(s):  
M. N. Ghabriel ◽  
J. J. Lu ◽  
W. H. Lim ◽  
B. P. Setchell
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Endothelial Cells ◽  
Ventral Prostate ◽  
Slight Reduction ◽  
Brain Endothelial Cells ◽  
Adult Rats ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Endothelial Barrier Antigen

It was recently shown that the endothelial barrier antigen (EBA), previously thought to be specific to endothelial cells in the central nervous system, was also present in endothelial cells in the testis and in epithelial cells in the dorsolateral prostate of adult rats.1 In the present study, we examined the effect of moderate spinal cord injury (SCI), produced by compression for 5 min of the cord at T 10/11. There was a slight reduction in EBA in the testis and prostate 24 h after SCI, and this became more obvious after 3days. EBA was completely absent from the prostate and testis at 1 week. By 2 and 4 weeks some expression of EBA returned, and at these times EBA was also detected in the ventral prostate. Brain endothelial cells remained positive throughout. We cannot yet say whether these changes are due directly to interference with the nerve supply, or involve changes in androgen status. (1)Ghabriel MN, Lu JJ, Hermanis G, Zhu C, Setchell BP (2002) Reproduction 123, 389–397.

ICI 176,334: A NOVEL NON–STEROIDAL, PERIPHERALLY SELECTIVE ANTIANDROGEN

1987 ◽  
Vol 113 (3) ◽  
pp. R7-R9 ◽  
Author(s):  
B.J.A. Furr ◽  
B. Valcaccia ◽  
B. Curry ◽  
J.R. Woodburn ◽  
G. Chesterson ◽  
...  
Keyword(s):  
Testosterone Propionate ◽  
Prostate Gland ◽  
Ventral Prostate ◽  
Adult Rats ◽  
Androgen Action ◽  
Serum Lh ◽  
Accessory Sex Organs ◽  
Hypothalamic Pituitary Axis ◽  
Rat Prostate ◽  
Higher Doses

ABSTRACT Pure antiandrogens, like flutamide, antagonize androgen action both peripherally and centrally at the hypothalamic–pituitary axis, which leads to an increase in LH and testosterone secretion. A new non–steroidal antiandrogen ICI 176,334 ((2RS)4′-cyano-3-(4-fluorophenylsulphonyl)-2-hydroxy-2-methyl-3′-trifluoromethyl)propion-anilide) has now been discovered which causes regression of the accessory sex organs but does not increase serum concentrations of LH and androgens. ICI 176,334 binds to rat prostate androgen receptors with an affinity around fourfold that of hydroxyflutamide. When administered s.c. concurrently with testosterone propionate (200μg/kg) for 7 days to immature castrated rats, ICI 176,334 (10mg/kg) significantly (P<0.001) inhibited growth of the seminal vesicles and ventral prostate gland. Oral administration of ICI 176,334 at doses of 1, 5 and 25mg/kg for 14 days to adult rats caused a dose–related reduction in accessory sex organ weights but had no effect on the testes. None of these doses caused a significant increase in serum LH and testosterone. Flutamide was around fourfold less potent and significantly increased serum LH and testosterone at the higher doses. ICI 176,334 was well tolerated. ICI 176,334 should, therefore, prove useful for the treatment of androgen–responsive benign and malignant diseases.

scholarly journals Bisphenol A Modifies the Regulation Exerted by Testosterone on 5α-Reductase Isozymes in Ventral Prostate of Adult Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Pilar Sánchez ◽  
Beatriz Castro ◽  
Jesús M. Torres ◽  
Asunción Olmo ◽  
Raimundo G. del Moral ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Prostate Gland ◽  
Ventral Prostate ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Adult Rats ◽  
Short Term Exposure ◽  
Rat Prostate ◽  
And Function ◽  
Dose Dependent

The development, growth, and function of the prostate gland depend on androgen stimulation. The primary androgen in prostate is 5α-dihydrotestosterone (DHT) which is synthesized from circulating testosterone (T) through the action of 5α-reductase (5α-R). Although 5α-R occurs as five isozymes, only 5α-R1 and 5α-R2 are physiologically involved in steroidogenesis. The endocrine disruptor bisphenol A (BPA) alters sexual organs, including the prostate. Our previous findings indicated that BPA decreased the expression of 5α-R1 and 5α-R2 in rat prostate but also circulating T. Thus, it is unclear whether BPA exerts this effect on 5α-R isozymes by reducing circulating T or by any other mechanism. In this study, we examine the effects of short-term exposure to BPA at doses below 25 μg/Kg/d and above 300 μg/Kg/d of the TDI on mRNA levels of 5α-R1 and 5α-R2 in prostate of adult castrated rats supplemented with T to achieve constant circulating T levels. mRNA levels were measured by absolute quantitative RT-PCR, T levels by RIA, and DHT levels by ELISA. Our results indicated that in castrated rats treated with T BPA at the two doses studied significantly decreased the mRNA levels of both 5α-R isozymes in a dose-dependent manner without modifications in circulating T.

scholarly journals Testosterone-stimulated growth of the rat prostate may be driven by tissue hypoxia and hypoxia-inducible factor-1α

2007 ◽  
Vol 196 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Stina Häggström Rudolfsson ◽  
Anders Bergh
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hypoxia Inducible Factor ◽  
Tissue Growth ◽  
Tissue Hypoxia ◽  
Ventral Prostate ◽  
Egfr Signaling ◽  
Adult Rats ◽  
Hypoxia Marker

Testosterone-stimulated growth of the ventral prostate (VP) in castrated rats is preceded by angiogenesis, but the mechanisms coordinating vascular and tissue growth are unknown. Adult rats were castrated and some treated with testosterone. Tissue hypoxia was studied morphologically using the hypoxia marker pimonidazole (Hypoxyprobe), hypoxia-inducible factor-1 (HIF-1) α, vascular endothelial growth factor (VEGF), and carbonicanhydrase 9 (CA-9) levels by western blotting and quantitative RT-PCR. In the intact untreated prostate, most glands were unstained by the hypoxia marker but already 1 day after castration most epithelial cells in the VP were stained. Seven days after castration prostate glands were apparently normoxic again, and HIF-1α, VEGF, and CA-9 were decreased. Treatment of 7-day castrated rats with testosterone resulted in increased epithelial hypoxyprobe staining and increased HIF-1α, VEGF, and CA-9 levels. The transient increase in tissue hypoxia after testosterone treatment is probably caused by a temporary mismatch between oxygen consumption and supply. Treatment of prostate epithelial cells in vitro under normoxic conditions also increased HIF-1α, and this could be blocked if epidermal growth factor receptor (EGFR) signaling was blocked with gefitinib. In vivo gefitinib could, however, not block the testosterone induced increase in HIF-1α. Testosterone may thus induce HIF-1α and its downstream angiogenesis promoting genes by at least two mechanisms, hypoxia and EGFR signaling. Transient epithelial cell hypoxia could by rapidly increasing HIF-1α and VEGF be an essential coordinator of testosterone-stimulated vascular and glandular growth.

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