Steroid Structure and Androgenic Activity

Liao, Shutsung; Liang, Tehming; Fang, Senmaw; Castañeda, Evangelina; Shao, Tsang-Cheng

doi:10.1016/s0021-9258(19)43521-7

Cited by 248 publications

(8 citation statements)

References 32 publications

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“…They reported that castrated male rats exposed to 17α-methyltestosterone, at a dose of 0.27 mg/day, had heavier seminal vesicle weights than those exposed to 0.27 mg/day of 19-nortestosterone. Similar results, reported as the relative androgenic activity of 17α-methyltestosterone and 19-nortestosterone, were demonstrated by Liao, Liang, Fang, Casteneda, and Shao (1973). Thus, 17α-methyltestosterone appears to be a potent stimulus for the sex accessory glands.…”

Section: Discussionsupporting

confidence: 80%

Comparison of the effects of 17 α–methyltestosterone, methandrostenolone, and nandrolone decanoate on the sexual behavior of castrated male rats.

Clark¹,

Fast²

1996

Behavioral Neuroscience

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In a series of 3 experiments, adult male Long-Evans rats were castrated and treated with 1 of 3 different anabolic-androgenic steroid (AAS) compounds (17 alpha-methyltestosterone, methandrostenolone, or nandrolone decanoate) for 6 weeks. In each experiment, subjects received daily injections of a high, medium, or low dose of AAS or the oil vehicle. The AAS effects on body weight in gonadectomized male rats were modest, and no effects on locomotor activity were observed. The AAS compounds administered at doses comparable with human abuse levels were not equipotent in maintaining male sexual behavior patterns (nandrolone decanoate > methandrostenolone > 17 alpha-methyltestosterone). In addition, the behavioral actions of AAS compounds did not parallel stimulation of sexual accessory glands. The authors reported that this study is the first to quantify the dose-response characteristics of individual AAS compounds with regard to these behavioral and endocrine measures.

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Section: Discussionsupporting

confidence: 80%

Comparison of the effects of 17 α–methyltestosterone, methandrostenolone, and nandrolone decanoate on the sexual behavior of castrated male rats.

Clark¹,

Fast²

1996

Behavioral Neuroscience

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“…DHT has a higher binding affinity to bloodstream circulation. Testosterone is converted into DHT by 5α-reductase in target organs, including the AR relative to testosterone (15,19,34). This observation suggested that the only difference between tes-the prostate (5,6).…”

Section: α-Reductasementioning

confidence: 99%

Inhibition of 5α-Reductase in Rat Prostate Reveals Differential Regulation of Androgen-Response Gene Expression by Testosterone and Dihydrotestosterone

et al. 2001

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“…Although antiandrogens are better studied, androgen disrupting chemicals can bind the AR and act as agonists or antagonists [26,42,60]. In addition to being modulated by ligands and having specific elements with high affinity, the AR is similar enough to the progestin and glucocorticoid receptor which allows to share response elements with them [54,[61][62][63]. The AR can also bind a variety of response elements on the DNA via the differing orientation of the homodimer formed after ligand binding to modulate a number of genes [63].…”

Section: Effects On Biological Pathwaysmentioning

confidence: 99%

Uncovering Evidence for Endocrine-Disrupting Chemicals That Elicit Differential Susceptibility through Gene-Environment Interactions

Wallis

Truong

et al. 2021

Toxics

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Exposure to endocrine-disrupting chemicals (EDCs) is linked to myriad disorders, characterized by the disruption of the complex endocrine signaling pathways that govern development, physiology, and even behavior across the entire body. The mechanisms of endocrine disruption involve a complex system of pathways that communicate across the body to stimulate specific receptors that bind DNA and regulate the expression of a suite of genes. These mechanisms, including gene regulation, DNA binding, and protein binding, can be tied to differences in individual susceptibility across a genetically diverse population. In this review, we posit that EDCs causing such differential responses may be identified by looking for a signal of population variability after exposure. We begin by summarizing how the biology of EDCs has implications for genetically diverse populations. We then describe how gene-environment interactions (GxE) across the complex pathways of endocrine signaling could lead to differences in susceptibility. We survey examples in the literature of individual susceptibility differences to EDCs, pointing to a need for research in this area, especially regarding the exceedingly complex thyroid pathway. Following a discussion of experimental designs to better identify and study GxE across EDCs, we present a case study of a high-throughput screening signal of putative GxE within known endocrine disruptors. We conclude with a call for further, deeper analysis of the EDCs, particularly the thyroid disruptors, to identify if these chemicals participate in GxE leading to differences in susceptibility.

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Steroid Structure and Androgenic Activity

Cited by 248 publications

References 32 publications

Comparison of the effects of 17 α–methyltestosterone, methandrostenolone, and nandrolone decanoate on the sexual behavior of castrated male rats.

Comparison of the effects of 17 α–methyltestosterone, methandrostenolone, and nandrolone decanoate on the sexual behavior of castrated male rats.

Inhibition of 5α-Reductase in Rat Prostate Reveals Differential Regulation of Androgen-Response Gene Expression by Testosterone and Dihydrotestosterone

Uncovering Evidence for Endocrine-Disrupting Chemicals That Elicit Differential Susceptibility through Gene-Environment Interactions

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