4.4 Article

Inflammatory repercussions in female steroid responsive glands after perinatal exposure to bisphenol A and 17-β estradiol

期刊

CELL BIOLOGY INTERNATIONAL
卷 45, 期 11, 页码 2264-2274

出版社

WILEY
DOI: 10.1002/cbin.11665

关键词

endocrine disruptor; female prostate; inflammation; mammary gland; morphology

资金

  1. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2018/23383-6, 2020/01240-9]
  2. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior [001]
  3. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo -Brazil (FAPESP) [2018/23383-6]

向作者/读者索取更多资源

The study evaluated inflammatory responses of the mammary gland and prostate to BPA and estradiol exposure, finding an increase in phospho-STAT3 positive cells and macrophages in the prostate of animals exposed to BPA, while the mammary gland did not show differences in inflammatory markers. The findings suggest that exposure to endocrine disruptors during the perinatal period leads to different inflammatory responses in reproductive organs, with the prostate being more susceptible to inflammatory mechanisms.
The mammary gland (MG) and female prostate are plastic reproductive organs which are highly responsive to hormones. Thus, endocrine disruptors, such as bisphenol A (BPA) and exogenous estrogens, negatively affect glandular homeostasis. In addition to previously described alterations, changes in inflammatory markers expression also trigger the development of a microenvironment that contributes to tumor progression. The current work aimed to evaluate the inflammatory responses of the MG and prostate gland to BPA (50 mu g/kg) and 17-beta estradiol (35 mu g/kg) exposure during the perinatal window of susceptibility. The results showed that at 6 months of age there was an increase in the number of phospho-STAT3 (P-STAT3) positive cells in the female prostate from animals perinatally exposed to 50 mu g/kg BPA daily. In addition, the number of macrophages increased in these animals in comparison with nonexposed animals, as shown by the F4/80 marker. Despite an increase in the incidence of lobuloalveolar and intraductal hyperplasia, the MG did not show any difference in the expression of the four inflammatory markers evaluated: tumor necrosis factor-alpha, COX-2, P-STAT3, and F4/80. Analysis of both glands from the same animal led to the conclusion that exposure to endocrine disruptors during the perinatal window of susceptibility leads to different inflammatory responses in different reproductive organs. As the prostate is more susceptible to these inflammatory mechanisms, it is reasonable to affirm that possible neoplastic alterations in this organ are related to changes in the inflammatory pattern of the stroma, a characteristic that is not evident in the MG.

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