Experimental alcoholism and pathogenesis of prostatic diseases in UChB rats
ABSTRACT Previous studies have shown that long-term alcohol treatment has negative effects on prostatic stromal-epithelial interaction. Thus, the aim of the present study was to analyze the histochemical, immunohistochemical and ultrastructural alterations that occur in the prostatic stroma and epithelium of rats submitted to chronic alcohol ingestion and alcohol abstinence, as well as to establish the relationship between these changes and prostatic diseases. Thirty male rats (10 Wistar and 20 UChB rats) were divided into three experimental groups: the control group received tap water, the alcoholic group received ethanol diluted to 10 degrees G.L. for 150 days, and the abstinent group received the same liquid diet as the alcoholic group up to 120 days of treatment and only tap water for 30 days thereafter. At the end of treatment, all animals were sacrificed and the ventral lobe of the prostate was removed and processed for histochemical, immunohistochemical and ultrastructural analyses. In addition, plasma testosterone levels were measured. The results showed prostatic intraepithelial neoplasia, infolding of the epithelium towards the stroma, stromal hypertrophy and the presence of inflammatory cells in alcoholic animals. In the abstinent group, alterations were noted mainly in the stromal area. In conclusion, ethanol triggers alterations in prostatic epithelial and stromal compartments, affecting the stromal microenvironment and predisposing the organ to pathological processes.
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ABSTRACT: Aquaporins (AQPs), notably AQP-1 and AQP-9, may contribute to reabsorption of fluid and solute across the epididymis. Ethanol is related to be a toxicant affecting directly or indirectly the epididymis and the sperm motility. This study examined the expression of AQP-1 and AQP-9 in adult epididymis of the UChA and UChB 10% (v/v) ethanol-preferring rats, focusing the ethanol-induced hormonal disturbances upon the regulation of these AQPs. Chronic ethanol intake significantly decreased body weight, while UChA and UChB rats displayed a marked loss of epididymal weights. Both ethanol-consuming animals had a severe reduction of testosterone levels, whereas LH and 17β-estradiol were unchanged. Throughout the epididymis, a strong reaction to AQP-1 was observed in myoid and endothelial cells of the UChB ethanol-preferring rats, differently from a moderate intensity in the initial segment of the UChA rats. In addition, AQP-9 showed a strong immunoreaction in the apical membrane of principal cells at initial segment. In cauda epididymis, the level of AQP-9 was reduced along the microvillus projections in both UChA and UChB rats compared to controls. We conclude that chronic ethanol consumption modulates the androgen levels, thereby modifying the expression pattern of AQP-1 and 9 in the epididymis.Tissue and Cell 11/2011; 44(1):47-53. DOI:10.1016/j.tice.2011.11.001 · 1.05 Impact Factor
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ABSTRACT: The aim of this work was to characterize the structural and molecular changes in the coagulating gland from rats submitted to long-term alcohol treatment, as well as the possibility of recovery of these parameters after interrupting the alcohol administration. Ten Wistar and twenty UChB rats were divided into: Control group received tap water; Alcoholic group received 10% (v/v) ethanol daily for 150 days; and Abstinent group, received 10% (v/v) ethanol daily for 120 days and then tap water like the control for another 30 days. After 150 days, samples from the coagulating glands were processed for morphological and immunohistochemical analyses. The results showed atrophied epithelium and hypertrophied stroma, especially in the alcoholic group. Intensed androgen receptor (AR) immunolocalization was verified in the epithelium and weak in the stroma of the control group in relation to the other groups. Intensed insulin-like growth factor receptor-1 (IGFR-1) immunolocalization was verified in the stroma of the alcoholic and abstinent groups. Thus, it could be concluded that the excessive alcohol consumption caused morphological and molecular changes in the coagulating gland, characterizing the inverse relation of AR and IGFR-1 localization. The alcohol was an important factor in cellular mitosis occurrence, which could be fundamental element involved in glandular lesions.Tissue and Cell 08/2010; 42(4):203-10. DOI:10.1016/j.tice.2010.04.001 · 1.05 Impact Factor
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ABSTRACT: The prostate is fundamental to the male reproductive process, and the stroma-epithelium interaction has an important role in prostate maintenance. Studies suggest that dystroglycan (DG) plays a role in cancer development in various organs. Thus, the aims of this work were to characterize morphological and proliferative features of the prostatic stroma and epithelium of mdx mice; to verify the immunolocalization of the α and β DG, IGF-1 and laminin α3 receptors; and to relate those structural and molecular events to prostate pathogenesis and to verify the viability of this experimental model in prostate studies. Thirty male mice (mdx and C57BL10/Uni) were divided into control and mdx groups. Samples from the ventral prostate were collected for immunological, Western Blotting, transmission electron microscopy and morphometric analyses. Oestradiol and testosterone measurements were verified. The results showed diminished testosterone and increased oestradiol levels in the mdx group. Atrophied cells and hypertrophied stroma were seen in the mdx mice. Weak α and β DG and laminin α3 immunolocalization was demonstrated in the mdx group. Intense insulin-like growth factor receptor α-1 (IGFRα-1) localization was identified in the mdx animals. Thus, mdx animals showed changes in molecular and structural integrity and proliferation signals, leading to glandular homoeostasis imbalance, and compromise of prostate function. Also, the steroid hormone imbalance and the increased IGF-1 receptor level detected in mdx mice could be considered as a crucial factor in the pathogenesis of prostatic disorders.International Journal of Experimental Pathology 10/2010; 91(5):408-19. DOI:10.1111/j.1365-2613.2010.00722.x · 2.05 Impact Factor