Disease relevance of C05290

• Plasma 19-hydroxyandrostenedione is elevated in patients with high renin essential hypertension [1].
• RESULTS: The basal levels of 19-hydroxyandrostenedione in Cushing's disease were elevated (mean +/- SD; 323 +/- 193 pmol/l, n = 13), while those in Cushing's syndrome due to adrenal adenoma were low (92 +/- 24 pmol/l, n = 7), compared to those in normal subjects (117 +/- 33 pmol/l, n = 54) [2].
• Low plasma 19-hydroxyandrostenedione levels in patients with aldosterone-producing adenoma [3].
• Because of the association of preeclampsia with hydatidiform mole, and since levels of 19-hydroxyandrostenedione (19-OH-A) and androstenedione (A) are raised in hypertensive diseases of pregnancy, we compared plasma 19-OH-A and A in hydatidiform mole patients with control early pregnant women [4].

High impact information on C05290

• Furthermore, the reactions catalyzed by these mutants were examined by evaluating the levels of the product estrone, and two intermediates, 19-hydroxyandrostenedione and 19-oxoandrostenedione by reverse phase high performance liquid chromatography using [7-3H]androstenedione as the substrate [5].
• Purified aromatase cytochrome P-450 displays catalytic characteristics similar to the enzyme in intact microsomes in the aromatization of androstenedione, 19-hydroxyandrostenedione and 19-oxoandrostenedione [6].
• Metabolism of 19-hydroxyandrostenedione in human subjects. Urinary excretion of conjugates [7].
• The 19-methyl analogues of androstenedione and its aromatization intermediates (19-hydroxyandrostenedione and 19-oxoandrostenedione) were evaluated as substrates of microsomal aromatase in order to determine the effect of a 19-alkyl substituent on the enzyme's regiospecificity [8].
• Enhancement of the hypertensinogenic action of 19-hydroxyandrostenedione by aromatase inhibitor, delta 1-testololactone [9].

Chemical compound and disease context of C05290

• The hypertensiogenic effects of 19-hydroxyandrostenedione (19-OH-A-dione) reported previously to be an amplifier of the action of aldosterone were evaluated using the same experimental procedures as for DOCA-salt hypertension in rats [10].
• A C19 steroid, 19-hydroxyandrostenedione (19-OHAD), an amplifier of the mineralocorticoid effects of aldosterone, is known to cause hypertension in rats during chronic administration [11].

Anatomical context of C05290

• 19-hydroxyandrostenedione does not modulate [3H]aldosterone binding to human mononuclear leucocytes and rat renal cytosol [12].
• 19-Hydroxyandrostenedione (19-OHA) is secreted from the adrenal glands in men and women and also from the placenta during pregnancy [13].
• Formation of 5(10)-estrene-3 beta,17 beta-diol, a novel 19-norsteroid, from androstenedione and 19-hydroxyandrostenedione by porcine granulosa cells is reported for the first time [14].
• The release of 3H2O from [1 beta-3H]testosterone by cultured cells was inhibited by the aromatizable androgens, 19-hydroxytestosterone and 19-hydroxyandrostenedione, indicating the specificity of the method for aromatization [15].
• Secretion of 19-hydroxyandrostenedione and 19-hydroxytestosterone by porcine Leydig cells in vitro and in vivo [16].

Associations of C05290 with other chemical compounds

• To verify the aldosterone amplifying action of 19-hydroxyandrostenedione (19-OH-AD), we investigated [3H]aldosterone and [3H]19-OH-AD binding to type I (mineralocorticoid) receptor in the renal cytosol of adrenalectomized and ovariectomized rat, and human mononuclear leucocytes (MNL) [12].
• Elevated plasma 19-hydroxyandrostenedione levels in Cushing's disease: stimulation with ACTH and inhibition with metyrapone [2].
• We investigated the effect of ACTH, angiotensin II (AII), and alpha-human atrial natriuretic polypeptide (alpha-hANP) which plays an important role of water-electrolytes balance, on 19-hydroxyandrostenedione (19-hydroxyandrost-4-ene-3,17-dione, 19-OH-A-dione) secretion by cultured human adrenal cells [17].
• 1,4,6-Androstatriene-3,17-dione did not inhibit the in vitro conversion of testosterone to 19-hydroxytestosterone by the testicular cell-free homogenates of the hCG-treated 18-day old rats, but strongly suppressed production of estrogen from 19-hydroxyandrostenedione [18].

Gene context of C05290

• OBJECTIVE: The regulation of 19-hydroxyandrostenedione secretion has been suggested to be under the control of both the ACTH-adrenal axis and renin-angiotensin system [2].
• Addition of purified NADPH-cytochrome P450 reductase to ROM decreased the accumulation of 19-hydroxyandrostenedione and increased the rate of estrone formation [19].
• Serum or serum plus FSH significantly stimulated (seven fold increase) formation of 5(10)-estrene-3 beta,17 beta-diol from androstenedione and 19-hydroxyandrostenedione [14].

Analytical, diagnostic and therapeutic context of C05290

• Serum level of 19-hydroxyandrostenedione during pregnancy and at delivery determined by gas chromatography/mass spectrometry [13].
• The hypertensinogenic effects of 19-hydroxyandrostenedione (19-OH-A-dione), which we reported as an amplifier of the action of aldosterone on the basis of the results obtained in bioassays using adrenalectomized rats, were evaluated in intact rats with both adrenals and kidneys [20].

References