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Highlights: [•] The HPA axis is a complex neuroendocrine loop that integrates stressor-related information. [•] Sex differences in the HPA axis arise through effects of gonadal steroid hormones. [•] Estrogen can alter HPA function though divergent actions mediated by ERalpha and ERbeta. [•] Androgens inhibit HPA function through actions at the androgen receptor or ERbeta. [ABSTRACT FROM AUTHOR]

Highlights: [•] DEHP and MEHP cause reproductive dysfunction in marine medaka. [•] DEHP and MEHP disturb the sex hormone balance. [•] DEHP and MEHP induce liver vitellogenin in male and change gonad histology. [•] DEHP and MEHP change the gene expressions of genes along the HPG axis. [•] The toxicity effects of DEHP are induced by DEHP itself and DEHP metabolites. [Copyright &y& Elsevier]

Abstract: Breast and prostate constitute organs of intense steroidogenic activity. Clinical and epidemiologic data provide strong evidence on the influence of androgens and estrogens on the risk of typical hormone-dependent malignancies, like breast and prostate cancer. Recent studies have focused on the role of androgen metabolites in regulating androgen concentrations in hormone-sensitive tissues. Steroid glucuronidation has been suggested to have a prominent role in controlling the levels and the biological activity of unconjugated androgens. It is well-established that serum levels of androgen glucuronides reflect androgen metabolism in androgen-sensitive tissues. Quantitative analysis of androgen metabolites in blood specimens is the only minimally invasive approach permitting an accurate estimate of the total pool of androgens. During the past years, androgen glucuronides analysis most often involved radioimmunoassays (RIA) or direct immunoassays, both methods bearing serious limitations. However, recent impressive technical advances in mass spectrometry, and particularly in high performance liquid chromatography coupled with mass spectrometry (LC–MS/MS), have overcome these drawbacks enabling the simultaneous, quantitative analysis of multiple steroids even at low concentrations. Blood androgen profiling by LC–MS/MS, a robust and reliable technique of high selectivity, sensitivity, specificity, precision and accuracy emerges as a promising new approach in the study of human pathology. The present review offers a contemporary insight in androgen glucuronides profiling through the application of LC–MS/MS, highlighting new perspectives in the study of steroids and their implication in hormone-dependent malignancies. [Copyright &y& Elsevier]

Abstract: Steroidogenic acute regulatory protein (StAR) mRNA levels in the eel ovary were assayed by quantitative PCR and related to plasma steroid levels throughout oogenesis in order to shed light on the previously considered ‘aberrant’ prematurational increase in plasma levels of estradiol-17β (E2). Total ovarian StAR transcript abundance mirrored circulating levels of E2, but not of 11-ketotestosterone (11KT). The study was complemented by evaluation of in vitro effects of follicle-stimulating hormone (FSH) on ovarian StAR transcript abundance and on short-term (‘acute’) radiolabelled pregnenolone-supported steroid metabolism by ovarian fragments to understand how the production of steroids during previtellogenic oocyte growth is regulated. We observed a significant effect of FSH on StAR mRNA levels within 24h of incubation, but these were no longer evident by 4 days of culture. Unexpectedly, FSH had no effect on substrate-supported steroidogenesis, as comparable yields of steroid products were detected using semi-quantitative HPLC and scintillation counting. We conclude that the eel ovarian follicle can respond to FSH from a very early stage of development (early oil droplet stage) by increasing StAR mRNA levels, but that there is no evidence for acute effects of FSH on bioactive steroid production downstream of cytochrome P450 side-chain cleavage. Furthermore, the prematurational increase in StAR mRNA in vivo is in keeping with general teleost models and is likely to be a ‘normal’ response to reaching advanced stages of development. [Copyright &y& Elsevier]

Highlights: [•] TGFβ1 increased human prostate stromal cell metabolism of DHEA to androgens. [•] Androstenedione and testosterone accumulated over time with increasing doses of TGFβ1. [•] TGFβ1 altered stromal cell expression of 3βHSD, and 17βHSD2 and 17βHSD5. [•] TGFβ1 did not increase androgen metabolism in prostate cancer cells (LAPC4). [•] Inflammation in prostate microenvironment may also increase androgenic metabolites. [ABSTRACT FROM AUTHOR]

Highlights: [•] Androgen deprivation therapy (ADT) is an effective treatment for prostate cancer. [•] We present a method for quantification of free and conjugated keto-androgens using SID-LC/ESI/SRM/MS. [•] This method was validated using standards set by the United States Food and Drug Administration (US FDA). [•] This was applied to patients enrolled in the Targeted Androgen Pathway Suppression (TAPS) clinical trial. [•] The method can be used to interrogate personalized response and resistance to ADT. [ABSTRACT FROM AUTHOR]