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• W2003341520 abstract "Specific blocks in the steroidogenic pathway involved in the production of testosterone by the Leydig cell can be irreversible due to the genetically determined absence of a specific enzyme, or reversible because of specific inhibitory effects of steroids. In the former case, the irreversible lesions are responsible for pathologically lower testosterone levels resulting in various forms of pseudohermaphroditism. In the latter case (caused by steroids), such inhibition is probably mediated via specific receptors in Leydig cells and may involve processes of transcription and translation. In the case of the reversible lesion, this may constitute a physiological mechanism by which the secretion of testosterone by the testis can be locally controlled, especially after periods of intense LH stimulation. The mediator of some of the most documented reversible lesions appear to be an oestrogen. In addition to such lesions, mechanisms causing the activation of specific metabolising enzymes also appear to play a role in the alteration of the secretory response under certain conditions. Finally the differential activation or inhibition of certain of the steroidogenic enzymes during development in various species may serve to alter testicular steroid secretion qualitatively, without affecting the steroidogenic potential of the cell. Such subtle alterations in the pattern of steroid secretion in certain species may, by altering the availability of biologically active androgens, serve to control the degree of peripheral androgenisation and the induction of puberty." @default.
• W2003341520 created "2016-06-24" @default.
• W2003341520 creator A5012152899 @default.
• W2003341520 creator A5023570210 @default.
• W2003341520 creator A5024613455 @default.
• W2003341520 date "1981-12-01" @default.
• W2003341520 modified "2023-10-14" @default.
• W2003341520 title "Regulation of steroidogenesis and steroid action in Leydig cells" @default.
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• W2003341520 doi "https://doi.org/10.1016/0022-4731(81)90261-2" @default.
• W2003341520 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7040817" @default.
• W2003341520 hasPublicationYear "1981" @default.
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