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PubMed1995

Use of an 18O2 inhalation technique and mass isotopomer distribution analysis to study oxygenation of cholesterol in rat. Evidence for in vivo formation of 7-oxo-, 7 beta-hydroxy-, 24-hydroxy-, and 25-hydroxycholesterol.

Cholesterol oxidation products (oxysterols) have been detected in many different tissues, often at concentrations 10(3) to 10(4) times lower than cholesterol. This constitutes a considerable risk of quantitation errors, since even a minor oxidation of cholesterol during sample processing would yield a substantial increase of oxysterol levels. It has therefore been suggested that some of the oxysterols do not occur in vivo and their detection in tissues merely are artifacts produced in vitro. In the present work, an 18O2 inhalation technique was developed in order to clarify which oxysterols are produced in vivo. Rats were exposed for 3 h to an atmosphere with a composition similar to normal air, except that it contained 18O2 instead of 16O2. Control rats were kept in 16O2-containing atmosphere throughout the experiment. The 18O enrichment of oxysterols in plasma and liver was determined by gas/liquid chromatography-mass spectrometry and mass isotopomer distribution analysis. In vivo formation of oxysterols, indicated by enrichment in 18O, was established for cholest-5-ene-3 beta, 7 alpha-diol, cholest-5-ene-3 beta, 7 beta-diol, 7-oxocholesterol, cholest-5-ene-3 beta,24-diol, cholest-5-ene-3 beta,25-diol, and cholest-5-ene-3 beta,27-diol. Additionally, it seems likely that cholest-5-ene-3 beta, 4 beta-diol is formed in vivo. The 18O labeling pattern suggests that there is incomplete equilibration between the liver and plasma pools of cholest-5-ene-3 beta,27-diol. No evidence for the in vivo formation of 5,6-oxygenated oxysterols was obtained.

Animals↗
PubMed1983

Progesterone production by hamster granulosa and luteal cells during short-term incubation. Effects of lipoproteins, compactin and 25-hydroxycholesterol.

Granulosa and luteal cells from immature, hormone-primed hamsters increased progesterone production in response to luteinizing hormone (LH) in a dose-dependent manner. Both cell types responded to 8-bromoadenosine 3':5'-cyclic monophosphate (8-Br-cAMP) with increased progesterone production. Lipoproteins (hamster or human) did not enhance progesterone production by either cell type in the presence of LH during short-term incubation; human high-density lipoprotein (HDL) inhibited progestin production. Compactin, an inhibitor of cholesterol biosynthesis, had no significant effect on progesterone production by either cell type. Granulosa and luteal cells increased progesterone production in response to 25-OH-cholesterol. The response to 25-OH-cholesterol was more rapid than that to LH. Increased progestin levels were apparent within 15 min of incubation whereas a response to LH was not seen until 30 min. LH in combination with 25-OH-cholesterol did not increase progesterone production above that seen with either agent alone. Cycloheximide blocked LH-stimulated steroidogenesis but not 25-OH-cholesterol-stimulated progestin production in both cell types. We conclude that 1) hamster granulosa and luteal cells rely upon endogenous, preformed cholesterol for the acute steroidogenic response to LH and 2) LH-stimulated steroidogenesis, but not 25-OH-cholesterol-stimulated steroidogenesis, is a cycloheximide-sensitive process which presumably involves an increase in the access of cellular cholesterol to the side-chain cleavage system.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1984

Effect of lipoproteins, 25-hydroxycholesterol and luteinizing hormone on in vitro follicular steroidogenesis in the hamster and rat.

In 4-h incubations with the medium changed every hour, proestrous Graafian follicles of the rat secreted greater amounts of progesterone (P4), androstenedione (delta) and estradiol (E2) than the hamster follicle (at H 1: 3.5, 3.6, 2.5 times, respectively). Follicles isolated from both species responded to 10-100 micrograms of human high-density lipoprotein (HDL) by enhanced P4 production, whereas these doses of HDL augmented delta and E2 secretion only in the hamster. One mg of human low-density lipoprotein (LDL) was as potent as 100 micrograms of HDL in stimulating P4 secretion in the hamster, but was unable to increase steroid synthesis in the rat. One to 50 micrograms of 25-hydroxy-cholesterol (25-OH) enhanced P4, delta and E2 secretion in a dose-dependent manner in the hamster follicle, but was without effect in the rat. In the hamster, 10-100 ng of luteinizing hormone (LH) increased steroid secretion in a dose-related fashion, while the rat follicle only responded to 100 ng of LH and the hamster follicle was much more responsive than the rat follicle. The responsiveness of the hamster follicle to 50 micrograms of 25-OH was less than to 100 ng LH (P4 production after LH stimulation was 12-fold greater than that after 25-OH stimulation). There was no additive effect of LH and HDL on follicular steroidogenesis in either species. A pharmacological dose of LDL (1000 micrograms) negated the stimulatory effect of LH on follicular steroidogenesis in both species, especially P4.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstenedione↗
PubMed2006

Perturbation of polyamine metabolism and its relation to cell death in human colon cancer cells treated by 7beta-hydroxycholesterol and 7beta-hydroxysitosterol.

7beta-OHsitosterol and 7beta-OHcholesterol are natural compounds of plant and animal cells with high structural similarity. Recently it was reported that both compounds induced apoptosis on human colon cancer cells by targeting different signalling pathways. Our study aimed at comparing their effects on polyamine metabolism and its relation to apoptosis. When human colon cancer cells were exposed to 7beta-OHsitosterol and to 7beta-OHcholesterol at concentrations inhibiting growth by the same degree, both compounds caused a reduction of polyamine biosynthetic enzyme activity, of the polyamine pools, and an increase of N1-acetylspermidine concentration indicating the enhancement of polyamine catabolism. Exogenous putrescine did not prevent cell death caused by 7beta-OHsitosterol, whereas 7beta-OHcholesterol-induced apoptosis was inhibited. MDL 72527, an inhibitor of polyamine oxidase, an enzyme of the polyamine catabolic pathway, potentiated the antiproliferative effects of 7beta-OHcholesterol by increasing the N1-acetylspermidine pool and enhanced the accumulation of apoptotic cells. In contrast, MDL 72527 did not change the apoptosis rate and the N1-acetylspermidine content in cells treated with 7beta-OHsitosterol. These data indicate that polyamine metabolic perturbations triggered by 7beta-OHcholesterol but not by 7beta-OHsitosterol are related to cell death.

Biogenic Polyamines↗
PubMed1989

[The role of gonadotropins, cyclic AMP, 22-R-hydroxycholesterol and cofactors in regulating endocrine functions of the Leydig cells in rats. II. Effects of LH, hCG, dbcAMP, 22-R-OH-cholesterol and cofactors on the synthesis of pregnenolone and testosterone in the interstitial gland of rats].

The authors examined in vitro the influence of gonadotrophins, cAMP, 22-R-OH-cholesterol and cofactors on the synthesis of pregnenolon and testosterone in the interstitial gland of the rat. Sections of the nucleus were incubated with LH (100 ng/ml), hCG (1.0 j.m./ml), dbcAMP (1 mM), 22-R-OH-cholesterol (30 microM) and cofactors (NAD + NADP + G-6-P + G-6-PDH). It was found that an increase in concentrations of hCG above physiological values was not accompanied by an increase in secreting steroid hormones. LH, hCG and dbcAMP increased the synthesis of pregnenolon twice, and testosterone--three times. 22-R-OH-cholesterol as a substrate increased the synthesis three and four times respectively, and added cofactors five times and four and a half times respectively. Joining 22-R-OH-cholesterol or a cofactor with LH does not intensify a stimulating effect.

Animals↗
PubMed1987

[In vitro study of the cytotoxicity and selectivity of 7 beta-hydroxycholesterol].

Since the mid seventies different groups of scientists have reported unanimously a cytotoxic effect of 7 beta-OH-cholesterol on tumor cell cultures. The effect on normal soma cells and a therewith associated possible tumor-specific selectivity however, is contrarily described. The present results confirm the cytotoxic effect of the substance against tumor cells. Further a high suppression in cell function of dividing soma cells by 7 beta-OH-cholesterol could be found. Thus the substance does not fulfill the hope for a selective drug in tumor therapy.

Cell Line↗