Alteration of cholesterol biosynthetic pathways in the skin of mice administered polycyclic aromatic hydrocarbons. (1/4)
When polycyclic aromatic hydrocarbons were applied solely or together with a tumor promoter (12-O-tetradecanoylphorbol-13-acetate) to the skin of mice, a marked decrease in the level of lathosterol was observed, reflecting a significant change in the metabolism of sterols. Yet the total amount of cholesterol was not changed. When diazacholesterol (a metabolic inhibitor) was administered to mice, both desmosterol and 5 alpha-cholesta-7,24-dien-3 beta-ol accumulated in the skin, whereas the level of lathosterol decreased. These results seem to suggest that a significant portion of lathosterol is formed via 5 alpha-cholesta-7,24-dien-3 beta-ol in addition to the pathway through methostenol. When polycyclic aromatic hydrocarbon was applied to the skin of the mouse treated with diazacholesterol, a significant increase of desmosterol and a marked drop of the level of 5 alpha-cholesta-7,24-dien-3 beta-ol were observed. These results strongly suggest that polycyclic aromatic hydrocarbons perturb the metabolism of sterol in the skin of mice while keeping the total amount of cholesterol unchanged. A similar metabolism also seems to be operating in tumor tissue itself. (+info)Metabolic interconversion of free sterols and steryl esters in Saccharomyces cerevisiae. (2/4)
The interconversion of free and esterified sterols was followed radioisotopically with [U-14C]acetate and [methyl-14C]methionine. In pulse-chase experiments, radioactivity first appeared mainly in unesterified sterols in exponential-phase cells. Within one generation time, the label equilibrated between the free and esterified sterol pools and subsequently accumulated in steryl esters in stationary-phase cells. When the sterol pools were prelabeled by growing cells aerobically to the stationary phase and the cells were diluted into unlabeled medium, the prelabeled steryl esters returned to the free sterol form under several conditions. (i) During aerobic growth, the prelabeled sterols decreased from 80% to 45% esters in the early exponential phase and then returned to 80% esters as the culture reached the stationary phase. (ii) Under anaerobic conditions, the percentage of prelabeled steryl esters declined continuously. When growth stopped, only 15% of the sterols remained esterified. (iii) In the presence of an inhibitor of sterol biosynthesis, which causes accumulation of a precursor to ergosterol, prelabeled sterols decreased to 40% steryl esters while the precursor was found preferentially in the esterified form. These results indicate that the bulk of the free sterol and steryl ester pools are freely interconvertible, with the steryl esters serving as a supply of free sterols. Furthermore, there is an active cellular control over what types of sterol are found in the free and esterified sterol pools. (+info)Effects of steroid blockers on LH-induced ovulation in the domestic fowl, Gallus domesticus. (3/4)
The spontaneous ovulation of hens was suppressed by daily injection of PMSG. The LH injected to overcome the block was accompanied by one of 4 compounds known to inhibit steroidogenesis at different sites in the biosynthetic pathway. A dose of 300 mg aminoglutethimide phosphate, which inhibits the conversion of cholesterol to 20 alpha-hydroxycholesterol, blocked the LH-induced ovulation and prevented the normal rise in plasma progesterone. Metyrapone, an inhibitor of 11 beta-hydroxylase, and SC 12937 and AY 9944, inhibitors of cholesterol synthesis, did not prevent ovulation or the progesterone rise induced by exogenous LH. Administration of progesterone overcame the inhibitory effect of aminoglutethimide, and it is suggested that progesterone is involved in the ovulatory process of the fowl. (+info)Effect of a chemical carcinogen and phorbol esters on sterol metabolism of mouse skin. (4/4)
The effect of 20-methylcholanthrene and phorbol esters on sterol metabolism of mouse skin was studied. When 4 beta-phorbol esters were administered to mice that were previously painted once with 20-methylcholanthrene, a depression of some sterols in skin occurred, of which that of lathosterol was most marked. This effect was not observed when the order of application was reversed. Using a metabolic inhibitor, diazacholesterol, it was shown that sterols which reduce in mouse skin by administration of carcinogen and promoters were similar to those which reduce by administration of carcinogen only and are the members of one of the two cholesterol-biosynthetic pathways, i.e., a pathway which proceeds through intermediates with a saturated side chain. The intensity of the lathosterol-depressing effect of phorbol esters depends on the order of application of 20-methylcholanthrene and promoters, the amount of promoters, molecular species of alcoholic moiety of esters, and configuration at C-4 of phorbol moiety. Of the phorbol esters tested, 4 beta-phorbol-12-myristate-13-acetate revealed the highest activity, which was followed by 4 beta-phorbol-12,13-didecanoate, 4 beta-phorbol-12,13-dibutyrate, 4 beta-phorbol-12,13-dibenzoate, 4 beta-phorbol-12,13-diacetate, 4 alpha-phorbol-12,13-didecanoate, and 4 alpha-phorbol. 4 alpha-Phorbol was practically inactive. When beta-naphthoflavone was substituted for 20-methylcholanthrene, little effect was observed except in TPA, which revealed a rather marked lathosterol-depressing activity. Phorbol esters themselves did show some activity of lathosterol depression without prior application of 20-methylcholanthrene, but the effects were much weaker. When anthralin was applied to mouse skin after the painting of 20-methylcholanthrene, a low but definite lathosterol-depressing effect was observed. (+info)
Donald Sharp Fredrickson, MD | Circulation
Sterol metabolism of micro-organisms | Biochemical Journal
Role of sterol metabolism in host response to virus (Durham)
Deep Sea Nasal Spray: Indications, Side Effects, Warnings - Drugs.com
Azacosterol
... (INN), or azacosterol hydrochloride (USAN) (brand name Ornitrol), also known as 20,25-diazacholesterol, is a ... Azacosterol acts as an inhibitor of 24-dehydrocholesterol reductase (24-DHCR), preventing the formation of cholesterol from ...
Triparanol
Azacosterol Desmosterolosis X-linked ichthyosis Clomestrone Mytatrienediol Elks J (14 November 2014). The Dictionary of Drugs: ...
Colestolone
Unlike late-stage cholesterol biosynthesis inhibitors like triparanol and azacosterol, no accumulation of sterols has been ...
Steroidogenesis inhibitor
24-Dehydrocholesterol reductase (24-DHCR) inhibitors such as azacosterol and triparanol inhibit the production of cholesterol ...
List of drugs: As-Az
... azacosterol (INN) Azactam azacyclonol (INN) azaftozine (INN) Azahexal (Hexal Australia) [Au], also known as azathioprine. ...
List of MeSH codes (D10)
... azacosterol MeSH D10.570.938.208.160 - cholestanol MeSH D10.570.938.208.222 - cholesterol, dietary MeSH D10.570.938.208.250 - ...
Bryant Park
... the BPC started scattering corn kernels that contained the drug azacosterol, which resulted in many pigeons becoming infertile ...
List of MeSH codes (D04)
... azacosterol MeSH D04.808.247.808.197.135 - cholestanol MeSH D04.808.247.808.197.200 - cholesterol esters MeSH D04.808.247.808. ... azacosterol MeSH D04.808.247.222.284.200 - cholesterol esters MeSH D04.808.247.222.284.478 - hydroxycholesterols MeSH D04.808. ...
MH DELETED MN ADDED MN
DeCS
English-Armenian Medical - Terms starting with 'Z' - MEDINDEX.AM
MH DELETED MN ADDED MN
MH DELETED MN ADDED MN
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DeCS 2014 - December 16, 2014 version
DeCS 2011 - December 22, 2011 version
DeCS 2008 - May 16, 2008 version
DeCS 2009 - February 20, 2009 version
DeCS 2010 - February 12, 2010 version
DeCS 2009 - February 20, 2009 version
DeCS 2013 - July 15, 2013 version
DeCS 2013 - December 17, 2013 version
DeCS 2008 - May 16, 2008 version
Hydroxycholesterols | Profiles RNS
Ory DS, Ottinger EA, Farhat NY, King KA, Jiang X, Weissfeld L, Berry-Kravis E, Davidson CD, Bianconi S, Keener LA, Rao R, Soldatos A, Sidhu R, Walters KA, Xu X, Thurm A, Solomon B, Pavan WJ, Machielse BN, Kao M, Silber SA, McKew JC, Brewer CC, Vite CH, Walkley SU, Austin CP, Porter FD. Intrathecal 2-hydroxypropyl-ß-cyclodextrin decreases neurological disease progression in Niemann-Pick disease, type C1: a non-randomised, open-label, phase 1-2 trial. Lancet. 2017 Oct 14; 390(10104):1758-1768 ...