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At least 973 records · Page 54Linked to original sources
PubMed1996

Peripheral benzodiazepine receptor ligands in rat liver mitochondria: effect on 27-hydroxylation of cholesterol.

The effect of peripheral benzodiazepine receptor ligands: PK11195 (1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)isoquinoline-3-carboxamid e), Ro 5-4864 (4-chlorodiazepam), hemin, N-methyl protoporphyrin IX and protoporphyrin IX on liver mitochondrial 27-hydroxylation of cholesterol was studied by adding them together with [4-14C]cholesterol. N-Methyl protoporphyrin IX, PK11195 and protoporphyrin IX stimulated mitochondrial 27-hydroxylation of [4-14C] cholesterol in vitro, the first two being the most potent (2-3-fold increase). Ro 5-4864 and hemin were not active. 27-Hydroxylation of [4-14C]cholesterol was reduced to below control levels (respectively 40 and 56% decrease compared to control, P < 0.01) when PK11195, N-methyl protoporphyrin IX or protoporphyrin IX were allowed to equilibrate in vitro with mitochondria for 20 min at 37 degrees C. Hepatic protoporphyria was induced using 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) (100 mg/kg, i.p.) to study the effect of in vivo accumulation of large amounts of dicarboxylic porphyrins, i.e. endogenous peripheral benzodiazepine receptor ligands, on cholesterol 27-hydroxylation. DDC treatment caused an increase in total porphyrin content in liver homogenate (10-fold) and mitochondria (2-fold). Mitochondrial 27-hydroxylation of [4-14C]cholesterol was depressed after treatment (60% decrease, P < 0.01). We suggest that peripheral benzodiazepine receptor ligands act on liver mitochondrial 27-hydroxylation of cholesterol by a mechanism coupled to these receptors and that the time of exposure of peripheral benzodiazepine receptors to ligands is a major factor. The modulation of 27-hydroxycholesterol production may have a physiological role in liver and possibly in other tissues.

Animals↗
PubMed1987

Rat liver cytosol oxysterol-binding protein. Characterization and comparison with the HTC cell protein.

A cytosol protein that specifically binds cholesterol derivatives oxygenated on the side chain has been demonstrated in rat liver and transformed HTC cells. This protein, of which the sedimentation coefficient is about 8 S, was saturable and showed a high binding affinity (Kd about 5 X 10(-9) M) for 25-hydroxycholesterol. Its molecular mass is about 160 kDa. The physicochemical characteristics of this protein were identical whether the model was normal or transformed. This oxysterol-binding protein differs from the well-known sterol carrier proteins.

Animals↗
PubMed1985

Steroidogenesis in ovarian cells of the Japanese quail (Coturnix coturnix japonica).

The influence of follicular maturation on steroidogenesis and steroid metabolism by isolated Japanese quail granulosa and theca cells was examined. When stimulated with LH, granulosa cells of the largest follicle (F1) responded with a sixfold increase over unstimulated progesterone levels, whereas progesterone production in cells of F3 less than doubled even when maximally stimulated. Forskolin stimulated progesterone synthesis in both F1 and F3 granulosa cells, but its effect was less pronounced than that of LH. Furthermore, F1 cells metabolized 25-hydroxycholesterol to a greater extent than did F3 cells. There was no appreciable metabolism of [3H]progesterone by granulosa cells. Theca cells from the smaller follicles (F3-F5) responded to LH stimulation with greater estrogen and androstenedione production than theca cells from F1. [3H]Progesterone was metabolized mainly to androstenedione in theca cells. Thus, the overall pattern of in vitro steroidogenesis in quail granulosa cells is similar to that described for the chicken and turkey even though the quantitative differences in the steroidogenic capacity between developing and mature follicles are more striking in the quail. Furthermore, although the LH-stimulated androstenedione and estrogen production appears similar in developing quail and chicken theca cells, the profile of [3H]progesterone metabolism is different in quail theca cells from that found previously in chicken theca cells.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Participation of the cytoskeleton in avian granulosa cell steroidogenesis.

Cytochalasin B (CB) and the more specific cytochalasin D (CD), disruptors of microfilament polymerization, and colchicine, an inhibitor of microtubule polymerization, were studied for their effects on cAMP and steroid production in granulosa cells of domestic fowl. Each agent was incubated with freshly dispersed cells from the largest preovulatory follicle of laying hens taken 3-4 hr before expected ovulation. Total content (cells + medium) of cAMP and steroids was measured by established radioimmunoassays. CB dose dependently inhibited basal as well as LH- and forskolin-stimulated cAMP generation and diminished basal, LH- and 25-hydroxycholesterol (25-OHC)-supported progesterone production. Conversely, CD potentiated LH- and forskolin-promoted cAMP generation as well as LH- and 25-OHC-stimulated progesterone synthesis. Neither drug had any influence on metabolism of pregnenolone to progesterone. Colchicine had no effect on cyclic AMP generation, yet it suppressed progesterone synthesis by inhibiting the conversion of pregnenolone to progesterone. beta-Lumicolchicine, a colchicine analog that does not depolymerize microtubules, had no such effect. The results suggest that microfilaments are involved in steroidogenesis at two sites, namely, the adenylate cyclase-cAMP system, and cholesterol conversion to pregnenolone; whereas microtubules act on the conversion of pregnenolone to progesterone.

Aminoglutethimide↗
PubMed1984

Properties of bovine luteal cytochrome P-450scc incorporated into artificial phospholipid vesicles.

Bovine luteal cytochrome P-450scc was purified and incorporated into artificial phosphatidylcholine vesicles. The vesicle reconstituted cytochrome used membrane bound cholesterol as substrate and cholesterol binding varied with the phosphatidylcholine fatty acyl composition and was stimulated by the presence of cardiolipin in the vesicle. 22R -hydroxycholesterol and 20 alpha, 22R - dihydroxycholesterol bound to the cytochrome up to 300 times more tightly than cholesterol and decreased the affinity of the cytochrome for CO by 100-200-fold. The properties of the cytochrome closely paralleled those reported for cytochrome P-450scc purified from the bovine adrenal gland.

Adrenal Glands↗
PubMed1995

Toxicity of oxidized low density lipoproteins for vascular smooth muscle cells and partial protection by antioxidants.

Oxidized low density lipoprotein (oxLDL) is known to be toxic to a variety of cell types, but relatively little is known about the toxic effects of oxLDL on vascular smooth muscle cells (SMC). We found that LDL oxidized by incubation with 5 microM cupric ions was toxic to cultured porcine SMC when administered at concentrations of 25 micrograms protein/ml and higher. The toxicity was demonstrated whether cells were proliferating or not, and was more evident in the presence of 0.4% lipoprotein-deficient serum than in 10%. Because of recent evidence that 7-ketocholesterol and 7-hydroxycholesterol are toxic species in copper-oxidized LDL, inhibition of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase was hypothesized as a mechanism of toxicity. However, mevalonic acid, the product of this enzyme, failed to protect against the toxicity of either oxLDL or the pure oxysterols. Alpha-tocopherol, alpha-tocopherol acetate, probucol, butylated hydroxytoluene, and deferoxamine provided partial protection to SMC exposed to oxLDL. These results suggested a toxic role for newly initiated lipid peroxidation, either in cells or in media oxLDL. Cellular lipid peroxidation appeared more likely, since no further oxidation of media oxLDL was demonstrated in the presence or absence of antioxidants. Overall, the results suggest that toxicity of copper-oxidized LDL for SMC is multifactorial and differs from the previously described toxicity of iron-oxidized LDL for fibroblasts.

Animals↗
PubMed1996

Dehydroepiandrosterone markedly inhibits the accumulation of cholesteryl ester in mouse macrophage J774-1 cells.

To clarify the antiatherogenic mechanism of action of dehydroepiandrosterone (DHEA), we investigated the effects of DHEA on the accumulation of cholesteryl ester (CE) in cultured mouse macrophage J774-1 cells. The accumulation of CE in J774-1 cells in the presence of acetyl low density lipoprotein (AcLDL) and 10(-5) mol/l DHEA was significantly reduced to 30% of the control values for 24 h. The marked effect of DHEA was observed as early as 6 h and continued at least for 48 h. This reduction by DHEA was dose-dependent and occurred starting at a DHEA dose of 5 x 10(-7) mol/1 for 24 h. DHEA treatment did not induced any changes in the cell surface binding, cell-association, or degradation of AcLDL. In comparison, the DHEA analogues, 8354 and 8356, which are known to be much stronger inhibitors of glucose 6-phosphate dehydrogenase than DHEA, did not show as marked an effect as DHEA on the accumulation of CE during the first 6 h. However, after 24-48 h of incubation, both 8354 and 8356 caused a marked reduction in the accumulation of CE similar to that observed with DHEA. A quantitative analysis of the cellular cholesterol content revealed that DHEA caused a marked reduction in CE with a concomitant continuous increase in free cholesterol (FC), while the DHEA analogues caused a marked reduction in CE with no change in FC. DHEA demonstrated little inhibitory effect on 25-hydroxycholesterol-driven esterification. Moreover, 10(-5) mol/1 DHEA induced a CE reduction in the foam cells induced by AcLDL. The CE-reducing capacity was also observed in the DHEA analogues. This CE-reducing capacity disappeared, however, when acyl CoA:cholesterol acyltransferase inhibitor, 58-035, was also present. Based on these findings, it can be concluded that the inhibitory effect of DHEA on the CE storage in response to AcLDL can be explained, at least in part, by two mechanisms. First, a recently published mechanism, namely, the inhibitory action of DHEA on lysosomal cholesterol transport, correlates well with the inhibition against foam cell transformation by DHEA in the early phase (at 6 h) observed in our study. With regard to the second mechanism, the CE-reducing capacity of DHEA from CE-laden foam cells, which appears to be related to a decreased cholesteryl ester cycle, may contribute to the inhibitory effect on the CE storage in the late phase (at 24 h and 48 h). These phase-specific inhibitory mechanisms of DHEA on the CE-storage may therefore partly explain the antiatherogenic action of DHEA.

Androstenes↗
PubMed1986

Site of gossypol inhibition of steroidogenesis in purified mouse Leydig cells.

Gossypol, a phenolic compound that has been studied as a potential male contraceptive, inhibits basal and LH-stimulated testosterone release from Leydig cells in vitro. The present study investigates the mechanism of this inhibition using preparations of purified mouse Leydig cells. Gossypol inhibited LH-stimulated progesterone, 17-hydroxyprogesterone and androstenedione production by mouse Leydig cells incubated in vitro. It also inhibited dibutyryl cyclic AMP-stimulated production of testosterone but was without effect in the presence of added pregnenolone or 25-hydroxycholesterol. These results suggest gossypol exerts its major inhibitory effect on Leydig cell function at a point between LH-dependent stimulation of cyclic AMP dependent protein kinase activity and increased availability of cholesterol for side chain cleavage.

17-alpha-Hydroxyprogesterone↗
PubMed1987

Regulation of low density lipoprotein receptor and cytochrome P-450scc mRNA levels in human granulosa cells.

hCG and 8-bromo-cAMP increase the levels of the mRNAs encoding the LDL receptor and cytochrome P-450scc in human granulosa cells. The increment in these mRNAs occurs rapidly after stimulation (within hours). Actin mRNA levels are not changed by hCG and 8-bromo-cAMP treatment. The tropic hormone effects on LDL receptor mRNA are observed even in the presence of 25-hydroxycholesterol and aminoglutethimide, which by themselves suppress LDL receptor mRNA. Actinomycin D blocks the hCG and 8-bromo-cAMP promoted augmentation of LDL receptor mRNA, suggesting that the tropic factors act to increase transcription of this gene. Treatment of cells with cycloheximide increases LDL receptor mRNA levels, and the stimulatory response to hCG and 8-bromo-cAMP is enhanced in the presence of cycloheximide. This indicates that tropic hormones act to increase LDL receptor mRNA levels without requiring synthesis of intermediary proteins and suggests that some short-lived protein may actually be reducing LDL receptors mRNA levels in these cells. We conclude that gonadotropins increase steroidogenesis in human granulosa cells, in part, by increasing expression of mRNAs encoding specific proteins involved in cholesterol metabolism.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1988

Control of bovine placental progestin synthesis: calcium dependent steroidogenesis is modulated at the site of the cholesterol side chain cleavage enzyme.

We have previously reported that progesterone synthesis in the bovine placenta is regulated by Ca2+ dependent and cyclic nucleotide independent mechanism. In studies conducted to further define the role of Ca2+ in the synthesis of progestins in bovine placental tissue, it was found that both protein kinase C (PKC), as determined by phosphorylation, and cytochrome P-450 side chain cleavage, as determined by Western blot analysis, were detectable in the steroidogenetically active portion of the placentome. To determine the site of action of PKC, fetal cotyledon cells were incubated in media containing 25-hydroxycholesterol in the absence or or presence of 10 ng/ml 12-O-tetradecanoyl-phorbol-13-acetate (TPA). It was found that TPA significantly (P less than 0.05) increased the conversion of the exogenous cholesterol analog to progesterone. To determine if the TPA could act synergistically with calcium activators, fetal cotyledon cells were incubated with either methyl isobutyl xanthine (MIX), an activator of intracellular calcium, or the calcium ionophore, A23187, which increases extracellular calcium influx, or both of these agents, in the presence or absence of TPA. It was found that TPA synergistically increased the conversion of sterol to progestins induced by submaximal concentrations of either MIX or A23187. In the presence of both compounds, TPA induced an even more dramatic increase in progestin synthesis. In experiments in which cyanoketone, an agent that inhibits the conversion of pregnenolone to progesterone, was added, TPA addition resulted in increased pregnenolone production, indicating that side chain cleavage of cholesterol is the site of action. The data, therefore, suggest that: (a) Ca2+ affects mechanisms regulating placental steroidogenesis; (2) one locus of Ca2+ is the cholesterol side chain cleavage reaction; and (3) PKC found in this tissue has a role in the Ca activated progestin production.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Production of C21 steroids in rat fetal ovaries.

Female gonads of fetal and neonatal rats were cultured for 24 h in medium 199 supplemented with dibutyryl cyclic AMP (dcAMP), cycloheximide, spironolactone (an inhibitor of 17 alpha-hydroxylase) or hydroxylated cholesterol derivatives. Radioimmunoassays of pregnenolone (P5) and progesterone (P4) were performed in the media. In control medium, progesterone production developed during the second week of life whereas ovaries treated with dcAMP (1 mM) produced progesterone as early as day 14.5 of gestation. The effect of the nucleotide was reversible and the lag period of responsiveness was 12 h. Cycloheximide (1 microgram/ml) added with dcAMP completely inhibited the production of progesterone. Addition of spironolactone to the basal medium was without effect but significantly increased P5 and P4 productions in the presence of dcAMP. The inhibitory effects of spironolactone and trilostane on steroidogenesis were tested in fetal testis. Lastly, the dcAMP effect could not be mimicked with hydroxylated cholesterol derivatives (20 microM). However, an additive effect of 22-hydroxycholesterol was observed in the presence of the nucleotide. These results indicate that the in vitro production of P5 and P4 by fetal ovaries in the presence of dcAMP suggests that dcAMP induces enzymes involved in C21 steroid synthesis. Levels of action of the nucleotide are discussed.

3-Hydroxysteroid Dehydrogenases↗
PubMed1988

Control of bovine placental progesterone synthesis: roles of cholesterol availability and calcium-activated systems.

It was previously reported that dispersed bovine placentome secretes progesterone and that the steroidogenic activity of these cells is stimulated by a calcium-mediated, cyclic nucleotide independent mechanism. In the present study, the influence of substrate availability was explored and the roles of calmodulin and protein kinase C in progestin production examined. Incubation of dispersed fetal cotyledon cells with 25-hydroxycholesterol (25-OH-C), a soluble sterol which readily enters cells and is metabolized to steroid hormones, increased progesterone secretion in a dose-dependent manner. The response to 25-OH-C was dependent on the extracellular calcium concentration. Methyl isobutyl xanthine (MIX) alone also increased pregnenolone as well as progesterone secretion, and the combination of 25-OH-C and MIX stimulated progesterone secretion was inhibited by trifluoperazine. The phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), caused no major effects on steroidogenesis but the stimulatory effects of MIX or the ionophore A23187 were enhanced in its presence. These findings suggest that (1) basal progesterone secretion by fetal cotyledon cells is limited by cholesterol availability; (2) MIX increases steroidogenesis in part by increasing the synthesis of pregnenolone, but its actions are expressed independently of cholesterol availability; (3) both calmodulin and protein kinase C may participate in the modulation of bovine placental steroidogenesis.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Influence of kaurenol on basal, LH- and forskolin-stimulated progesterone and cAMP production in avian granulosa cells.

The effects of kaurenol, a diterpene alcohol, were evaluated on progesterone and cyclic AMP (cAMP) production in freshly dispersed avian granulosa cells. Kaurenol (50 microM) alone caused a fourfold increase in progesterone synthesis without a measurable influence on cAMP levels. When granulosa cells were challenged with near-maximally stimulating concentrations of LH (50 ng/ml) or forskolin (10 microM), kaurenol (10-100 microM) dose-dependently suppressed steroidogenesis. Similarly, cAMP production in response to LH and forskolin stimulation was also inhibited. When progesterone synthesis was stimulated by the addition of pregnenolone or 25-hydroxycholesterol substrates to the culture medium, the typical dose response to the latter precursor, but not to pregnenolone, was abolished by kaurenol. Whereas the mechanism of kaurenol's stimulatory effect on basal steroidogenesis remains unknown, it is suggested that its inhibitory action on LH- and forskolin-promoted progesterone production may be due to the inhibition of the adenylate cyclase cAMP effector system as well as to the impairment of the action of the mitochondrial cholesterol side chain cleavage enzyme system.

Animals↗
PubMed1976

Intermediates in the conversion of cholesterol to pregnenolone: kinetics and mechanism.

The early kinetics of the conversion of cholesterol (A) to (22R)-22-hydroxycholesterol (B), (20R,22R)-20,22-dihydroxycholesterol (C) and pregnenolone (D) has been studied with bovine adrenocortical mitochondrial aceton-dried powder preparations. The sequential appearance of B, C, and D was demonstrated. During the lag period of D appearance, B, and C approached steady state levels, at which time the formation of D approximated linearity. The initial rate of B appearance approximated the rate of the linear phase of pregnenolone formation. When cholesterol was initially incubated in an 18O2-enriched atmosphere, the gas phase abruptly changed to air and incubation continued for a relatively short period, there was a drop in the 18O content of the recovered B and C. These results demonstrated for the first time the turnover of these compounds as they formed in the system from cholesterol, without the use of exogenously added tracer B or C. The 18O content of the recovered glycol was lower at position C-20 than at C-22, as would be expected from a consecutive process involving an initial oxygen attack of cholesterol at C-22. These results suggest the sequence A leads to B leads to C leads to D as the basic mechanism for the conversion of cholesterol to pregnenolone.

Adrenal Cortex↗
PubMed1995

Stimulation of progesterone secretion in dispersed cells of rat corpora lutea by antioxidants.

Antioxidants were used to investigate the role of free radicals in control of luteal steroidogenesis. Corpora lutea from pseudopregnant rats were enzymatically dispersed, the cells were incubated with antioxidants, and progesterone production was measured. Addition of the antioxidants nordihydroguaiaretic acid (NDGA), butylated hydroxytoluene (BHT), and the gonadotropin luteinizing hormone (LH) resulted in a dose-dependent increase in progesterone secretion. However, the response pattern to these treatments differed with the age of the corpora lutea, and unlike LH neither NDGA nor BHT treatment resulted in an increase in the intracellular second messenger cAMP. Nevertheless, LH and antioxidant-induced progesterone stimulation could be blocked by the addition of either aminoglutethimide or ketoconazole, cytochrome P450 side-chain cleavage (cytochrome P450 SCC) enzyme inhibitors, which prevent the conversion of cholesterol to pregnenolone and thus block steroid hormone synthesis. Also, unlike exposure to LH, exposure to antioxidants resulted in an additional increase in progesterone production in luteal tissue saturated with 25 hydroxycholesterol, a soluble cholesterol analog which serves as a substrate for cytochrome P450 SCC. This study suggests that the site of antioxidant action in affecting progesterone secretion may be at the cytochrome P450 SCC enzyme. Based on these results and on studies in other steroid hormone-producing cells, it appears that free radicals may be involved in regulating synthesis by modulating activity of cytochrome P450 SCC enzyme in rat luteal tissue.

Animals↗
PubMed1994

Heat shock protein induction blocks hormone-sensitive steroidogenesis in rat luteal cells.

A variety of agents induce heat shock proteins (HSPs) in addition to heat shock. The heat shock response and its effects on luteal function have not been investigated, but provocatively, many of the agents known to induce HSPs impair progesterone synthesis in luteal cells. We therefore investigated whether HSP induction might influence luteal function. Rat luteal cells exposed to a commonly used heat shock paradigm (45 degrees C; 10 min) were shown to induce HSP of 70 kDa (HSP-70). Heat shock also caused a complete abrogation of LH-sensitive progesterone and 20 alpha-dihydroprogesterone secretion, and blocked steroidogenesis in response to 8-bromo-cAMP and forskolin. In contrast, heat shock had no effect on cAMP accumulation in response to LH or forskolin, or on basal progestin secretion. Heat shock inhibition of steroidogenesis was fully reversed by 22R-hydroxycholesterol (22-OH cholesterol), a cell- and mitochondria-permeant cholesterol analog. Inhibition of transcription with actinomycin D blocked HSP-70 induction and significantly reversed the inhibition of steroidogenesis by heat shock treatment. The antisteroidogenic response of heat shock was coincident with induction of HPSs and both events were transcription dependent. These findings provide strong evidence that HSP induction inhibits steroidogenesis. The mechanism of the antisteroidogenic action of HSP induction appears to be due to interference with translocation of cholesterol to mitochondrial cytochrome P450scc, a conclusion based on reversal of inhibition by 22-OH cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Effect of cadmium and other metal cations on in vitro Leydig cell testosterone production.

In vivo assessment of toxicant action on Leydig cell function is subject to homeostatic mechanisms which make it difficult to determine whether any changes seen in serum testosterone (T) concentration are due to extragonadal endocrine alterations or to a direct effect on the Leydig cell. For example, metal cations administered in vivo have been shown to depress serum T concentration and alter serum concentrations of pituitary hormones in laboratory animals. The studies reported here use a testicular cell culture technique to evaluate Leydig cell testosterone biosynthesis in the presence of several metal cations. To determine the site of toxic action, the Leydig cells were stimulated to produce testosterone by using human chorionic gonadotrophin (hCG), dibutyl cyclic adenosine monophosphate (db-cAMP), or several substrates required for the biosynthesis of testosterone. hCG was chosen because resultant T production requires an intact membrane receptor and db-cAMP was used to test for post LH receptor defects caused by the metals. The other substrates were chosen to isolate the effect of metals on enzymatic pathways. Collagenase dispersed testicular cells (15% Leydig cells) were incubated with metal cations (1 to 5000 microM) for 3 hr in the absence and presence of maximally stimulating concentrations of hCG, db-cAMP, 20 alpha-hydroxycholesterol (HCHOL), or pregnenolone (PREG), and T concentration was determined by radioimmunoassay. In one separate experiment we also tested the effect of the substrates progesterone, 17 alpha-hydroxy-progesterone, and androstenedione on Cd2(+)-treated Leydig cells. The results show no change in Leydig cell viability with any metal cation treatment during the 3-hr incubation. Ca2+, Cr3+, Fe3+, Mg2+, Na+, or Pb2+ had no effect on stimulated testosterone. Dose-response depression in both hCG- and db-cAMP-stimulated T production were seen with Cd2+, Co2+, Cu2+, Hg2+, Ni2+, and Zn2+ treatment. Surprisingly, Cd2+, Co2+, Ni2+, and Zn2+, which caused a depression in hCG- and db-cAMP-stimulated T production, caused significant increases in HCHOL- and PREG-stimulated T production over untreated and similarly stimulated cultures. This indicates that these cations may act at multiple sites within the Leydig cell.

17-alpha-Hydroxyprogesterone↗