Description
Principle of the assay: This assay employs the competitive inhibition enzyme immunoassay technique. The microtiter plate provided in this kit has been pre-coated with an antibody specific to 11-Deoxycortisol. Standards or samples are added to the appropriate microtiter plate wells with biotin-conjugated 11-Deoxycortisol. A competitive inhibition reaction is launched between 11-Deoxycortisol (Standards or samples) and biotin-conjugated 11-Deoxycortisol with the pre-coated antibody specific for 11-Deoxycortisol. The more amount of 11-Deoxycortisol in samples, the less antibody bound by biotin-conjugated 11-Deoxycortisol. After washing, Streptavidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Substrate solution is added to the wells and the color develops in opposite to the amount of 11-Deoxycortisol in the sample. The color development is stopped and the intensity of the color is measured.
Background: Cortodoxone (INN, USAN, BAN), also known as 11-deoxycortisol, 17-hydroxy-11-deoxycorticosterone, and 17alpha,21-dihydroxyprogesterone, as well as cortexolone, is aglucocorticoid steroid hormone that can be oxygenated to cortisol (hydrocortisone). It was first synthesized by Tadeusz Reichstein, and has also been referred to as Reichstein's Substance. On April 5, 1952, biochemist Durey Peterson and microbiologist Herbert Murray at Upjohn published the first report of a breakthrough fermentation process for the microbial 11alpha-oxygenation of steroids (e.g. progesterone) in a single step by common molds of the order Mucorales. 11alpha-oxygenation of cortodoxone produces 11alpha-hydrocortisone, which can be chemically oxidized tocortisone, or converted by further chemical steps to cortisol. Subsequent fermentation processes for the microbial 11beta-oxygenation of steroids in a single step were developed that could convert cortodoxone directly to cortisol. Cortodoxone functions as a glucocorticoid, though is less potent than cortisol. It can be synthesized from 17-hydroxyprogesterone. In 11beta-hydroxylase deficiency, cortodoxone levels increase dramatically, causing hypertension (as opposed to 21alpha-hydroxylase deficiency, in which patients have hypotension from a lack of mineralocorticoids). Cortodoxone can also be converted to androstenedione. This could explain, at least in part, the marked increase in androstenedione levels in 11beta-hydroxylase deficiency