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Estrogen and Androgen Blockade for Advanced Prostate Cancer in the Era of Precision Medicine
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Tetsuya Fujimura, Kenichi Takayama, Satoru Takahashi, Satoshi Inoue
Initially, the action of estrogens was believed to be mediated via the blockade of the pituitary–testicular axis, which effectively decreased circulating androgen levels and induced tumor regression. This concept was supported by immunohistochemical and in situ hybridization studies conducted in the 1990s, which could not identify any detectable estrogen receptor (ER) levels in the epithelial compartments of the human prostatic tissue [6]. The classical ER, ERα, is dominantly expressed in the stromal compartment but not in the glandular epithelium of the normal human prostate [6–8]. Estrogens actions on prostatic epithelium have been considered to be exerted via ERα-mediated paracrine mechanism. Conversely, the exposure of humans or rodents to estrogens induced proliferative changes and squamous metaplasia in their prostates [9–11]. Noble strain rats treated with androgen plus estrogens over a long period have been reported to show high PC incidence [12]. The mechanism underlying estrogen action was clarified in the past two decades owing to the successful cloning of nuclear receptors, such as ERα, ERβ, and estrogen-related receptors (ERRs: ERRα, ERRβ, and ERRγ) from 1980 to 1996 [13–16]. Evidence suggests an overlap between ERR and ER biology.
Estrogen and Androgen Blockade for Advanced Prostate Cancer in the Era of Precision Medicine
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2019
Tetsuya Fujimura, Kenichi Takayama, Satoru Takahashi, Satoshi Inoue
Initially, the action of estrogens was believed to be mediated via the blockade of the pituitary–testicular axis, which effectively decreased circulating androgen levels and induced tumor regression. This concept was supported by immunohistochemical and in situ hybridization studies conducted in the 1990s, which could not identify any detectable estrogen receptor (ER) levels in the epithelial compartments of the human prostatic tissue [6]. The classical ER, ERα, is dominantly expressed in the stromal compartment but not in the glandular epithelium of the normal human prostate [6–8]. Estrogens actions on prostatic epithelium have been considered to be exerted via ERα-mediated paracrine mechanism. Conversely, the exposure of humans or rodents to estrogens induced proliferative changes and squamous metaplasia in their prostates [9–11]. Noble strain rats treated with androgen plus estrogens over a long period have been reported to show high PC incidence [12]. The mechanism underlying estrogen action was clarified in the past two decades owing to the successful cloning of nuclear receptors, such as ERα, ERβ, and estrogen-related receptors (ERRs: ERRα, ERRβ, and ERRγ) from 1980 to 1996 [13–16]. Evidence suggests an overlap between ERR and ER biology.
Antiinflammatory effect of the ethanolic extract of Korean native herb Potentilla rugulosa Nakai in Bisphenol-a-stimulated A549 cells
Published in Journal of Toxicology and Environmental Health, Part A, 2023
Yong Geon Choi, Won Seok Choi, Jin Yong Song, Yubin Lee, Su Hyun Lee, Jong Seok Lee, Sarah Lee, Se Rin Choi, Choong Hwan Lee, Ji-Yun Lee
Bisphenol A (BPA), a component of epoxy resin and polycarbonate plastics (Tsai 2006), is widely used to manufacture various products, including bottles, bowls, card receipts, and dental sealants (Staples et al. 1998). Thus, the risk of environmental exposure to BPA has increased with elevated usage of BPA-based products (Kang, Kondo, and Katayama 2006). In particular, BPA acts as an EDC in mammals and humans, where this compound functions as a xenoestrogen binding to estrogen-related receptor γ (ERRγ) (Takayanagi et al. 2006; Yoon et al. 2014). In women, BPA produces obesity, abortion, infertility, polycystic ovarian hypertrophy, and adverse effects on the endometrium (Chianese et al. 2018; Kawa et al. 2021; Manikkam et al. 2013) Sexual dysfunction was also reported in males including occupationally exposed individuals to BPA (Campos et al. 2019; Chianese et al. 2018; Li et al. 2009). Although the major routes of BPA exposure are skin contact and dietary intake, inhalation is also an important route for exposure (Huang et al. 2012). BPA exposure is associated with an increased risk of bronchial hypersensitivity, wheezing, and asthma in adults (Robinson and Miller 2015). However, the association between BPA exposure and childhood asthma is controversial (Wu et al. 2021; Xie et al. 2016; Yang et al. 2020).
Systems toxicology approach explores target-pathway relationship and adverse health impacts of ubiquitous environmental pollutant bisphenol A
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Manigandan Nagarajan, Gobichettipalayam Balasubramaniam Maadurshni, Jeganathan Manivannan
Computational toxicology integrates experimental data and computer-based models to predict the adverse health effects induced by chemicals, such as environmental pollutants (Reisfeld and Mayeno 2012; Yamagata, Yamada, and Horii 2019; Luechtefeld and Hartung 2017). With respect to the aspect of docking, an earlier study performed by Babu et al. (2012) found that the molecular docking of BPA and its nitrated and chlorinated metabolites onto human estrogen-related receptor-gamma. Ikhlas, Usman, and Ahmad (2019) demonstrated the interactions between BPA and its endocrine disrupting analogues with bovine serum albumin using multi-spectroscopic and molecular docking studies.
Adverse health effects and stresses on offspring due to paternal exposure to harmful substances
Published in Critical Reviews in Environmental Science and Technology, 2023
Jiaqi Sun, Miaomiao Teng, Fengchang Wu, Xiaoli Zhao, Yunxia Li, Lihui Zhao, Wentian Zhao, Keng Po Lai, Kenneth Mei Yee Leung, John P. Giesy
One epigenetic mechanism, methylation of DNA, is considered to be a more stable epigenetic marker, so it has been widely studied as a candidate mediator of sperm-mediated phenotypes. Exposure to harmful substances has also been shown to affect the methylation of DNA in sperm (Anway et al., 2005; Teng et al., 2020a; Teng et al., 2020b). Analysis of sperm produced by F3 offspring of paternal mice that had been exposed to a mixture of endocrine disruptor compounds BPA, bis(2-ethylhexyl) phthalate (DEHP), and dibutyl phthalate (DBP) derived from plastics showed differential methylation regions in the promoters of genes related to metabolic disorders, such as glial cell derived neurotrophie (Gdnf), fibroblast growth factor 19 (Fgf19) and estrogen related receptor alpha (Esrra) (Manikkam et al., 2013). When detecting the molecular basis of intergenerational male infertility in mice, changes in the epigenome and transcriptome were found in testicular Sertoli cells of the F3 generation mice after ancestral exposure to the fungicide vinclozolin (Guerrero-Bosagna et al., 2013). Several known differentially regulated genes, such as histone deacetylase 1 (Hdac1) and heat shock protein 90 alpha family class A member 1 (Hspaa1), are associated with male infertility (Pastuszak & Lamb, 2012). These transgenerational phenotypes were correlated with changes in the methylation of DNA in sperm of the F3 generation. Most behavioral changes were further manifested in male offspring separated from their mothers, although these males were normal (Franklin et al., 2010). Long-term isolation from mothers also changed the methylation of DNA in the promotor regions of several candidate genes, such as methyl CpG binding protein 2 (Mecp2) and cannabinoid 1 (Cb1), in these isolated male germ lines (Franklin et al., 2010).