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・ 5-11 Campaign
・ 5-12
・ 5-25-77
・ 5-3-2
・ 5-4-3 rule
・ 5-4-3-2-Run
・ 5-5 duoprism
・ 5-7-9
・ 5-alpha reductase
・ 5-alpha-reductase deficiency
・ 5-alpha-reductase inhibitor
・ 5-amino-6-(5-phosphoribosylamino)uracil reductase
・ 5-Aminoimidazole ribotide
・ 5-aminopentanamidase
・ 5-aminovalerate transaminase
5-Androstenediol
・ 5-Androstenedione
・ 5-APB
・ 5-APDB
・ 5-APDI
・ 5-Benzyloxytryptamine
・ 5-beta-reductase
・ 5-Bromo-4-chloro-3-indolyl phosphate
・ 5-Bromo-DMT
・ 5-Bromouracil
・ 5-Bromouridine
・ 5-Carboxamidotryptamine
・ 5-carboxymethyl-2-hydroxymuconate Delta-isomerase
・ 5-carboxymethyl-2-hydroxymuconic-semialdehyde dehydrogenase
・ 5-cell


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5-Androstenediol : ウィキペディア英語版
5-Androstenediol

Δ5-Androstenediol (abbreviated as Δ5-diol), commonly referred to simply as androstenediol, and also known as androst-5-ene-3β,17β-diol, is an endogenous androgen and estrogen steroid hormone and intermediate in the biosynthesis of testosterone from dehydroepiandrosterone (DHEA).
Δ5-Diol is a direct metabolite of the most abundant steroid produced by the human adrenal cortex, DHEA. It is less androgenic than the related compound, Δ4-androstenediol, and has been found to stimulate the immune system. When administered to rats, Δ5-diol, ''in vivo'', has approximately 1.4% of the androgenicity of DHEA, 0.54% of the androgenicity of androstenedione, and 0.21% of the androgenicity of testosterone.〔Coffey, DS (1988) "Androgen action and the sex accessory tissues". In E Knobil, J Neill (eds), The Physiology of Reproduction. Raven Press, New York, pp 1081-1119.〕
Δ5-Diol possesses potent estrogenic properties, similarly to DHEA and 3β-androstanediol.
==Use as radiation countermeasure==
The value of Δ5-diol as a radiation countermeasure is based mainly on its stimulation of production of white blood cells and platelets.〔 Its potential use as a radiation countermeasure was introduced by the Armed Forces Radiobiology Research Institute (AFRRI) and subsequently studied by AFRRI and Hollis-Eden Pharmaceuticals under the tradename Neumune for the treatment of acute radiation syndrome.
The clinical trials with rhesus monkeys was successful. According to the Hollis-Eden report, only 12.5% of the 40 Neumune-treated animals died versus 32.5% in the placebo group.〔 (Hollis-Eden Pharmaceuticals Reports Publication of Results Demonstrating the Ability of NEUMUNE(R) to Increase Survival in a Primate Model of Lethal Radiation Injury ), February 26, 2007.〕
Hollis-Eden had applied for a contract from the U.S. Government under the BioShield Request for Proposals (RFP) for radiation countermeasures. After being encouraged for 2.5 years that Neumune was in the competitive range, on March 9, 2007, the RFP was canceled by HHS. According to HHS, "the product was no longer in the competitive range".〔(Government Nukes Hollis-Eden's Radiation Drug ), by Val Brickates Kennedy and Angela Moore, March 8, 2007〕〔(US cancels radiation contract with Hollis-Eden ), March 9, 2007〕 No further explanation was given. As a result, Hollis-Eden has now withdrawn from the radiation countermeasure field.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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