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Results for “Hydroxycholesterols”

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At least 343 records · Page 19Linked to original sources
PubMed1981

The transfer of cholesterol and hydroxycholesterol derivatives from liposome to soluble cytochrome P-450 scc.

We have studied the cholesterol-binding reaction with purified steroid-free cytochrome P-450scc. By mixing an aqueous solution of cholesterol-, pregnenolone- and progesterone-free cytochrome with cholesterol-containing liposomes, the low to high spin conversion of the hemoprotein was observed spectrophotometrically and by electron spin resonance spectroscopy. When the binding rates were compared at a fixed molar heme: cholesterol ratio of 1 : 1, 20 mol% cholesterol-dioleoylglycerophosphocholine liposomes react with the cytochrome at a faster rate than 50 mol% cholesterol-dimyristoylglycerophosphocholine liposomes, indicating that the availability of cholesterol molecules in an unsaturated membrane is better than in a saturated membrane. When the number of cholesterol-dioleoylglycerophosphocholine liposomes was increased, the cholesterol-binding rates increased markedly. These results imply that the collision of the liposomes with the soluble hemoprotein molecules plays an important role in the binding reaction under our experimental conditions. The binding reaction was found to be temperature-dependent with a refractive temperature at near 20 degrees C. From the comparison of the binding abilities among cholesterol derivatives tested, wer conclude that the alpha-face of the A-B transfused rings and the portion of the hydrocarbon side-chain of cholesterol are important for the binding. Additionally, polar derivatives had faster rates than non-polar steroids in structurally homologous series.

Adrenal Cortex↗
PubMed1990

Metabolism of 7 beta-hydroxycholesterol in astrocyte primary cultures and derived spontaneously transformed cell lines: correlation between the esterification on C-3 -OH by naturally occurring fatty acids and cytotoxicity.

The lethal effect of 7 beta-hydrocholesterol (7 beta-OHC) on spontaneously transformed cell lines, derived from neonatal rat astrocyte primary cultures and the extent of 7 beta-OHC esterification by naturally occurring fatty acids on C-3 -OH (metabolite) was investigated. The extent of cellular death and metabolite biosynthesis matched with the 7 beta-OHC concentrations. Incubation of the cells with 10 microM 7 beta-OHC in the presence of either lipoproteins depleted fetal calf serum or with increasing serum concentrations revealed proportionality between the degree of cellular cytotoxicity and metabolite levels. The use of tetracaine or progesterone as acyl-CoA: cholesterol acyltransferase (ACAT) inhibitors indicated that ACAT was involved in metabolite production; the inhibition of metabolite biosynthesis slowed down 7 beta-OHC lethal effect. Incubation of the cells with 1 mM db-cAMP, prior 7 beta-OHC treatment, enhanced both metabolite production and cellular death. These findings support the view that the metabolite is directly implicated in the cytotoxic action.

Animals↗
PubMed1988

Effect of 7 beta-hydroxycholesterol on growth and membrane composition of Mycoplasma capricolum.

7 beta-OH cholesterol in a cholesterol rich growth medium (5-10 micrograms/ml) extended the lag period and slowed down the growth rate of Mycoplasma capricolum cells. In a cholesterol poor medium (0.5 micrograms/ml) inadequate to support growth, 7 beta-OH cholesterol exerts a synergistic effect on growth. The 7 beta-OH cholesterol was incorporated unchanged from the growth medium and could be recovered exclusively in the membrane fraction. The incorporation of the 7 beta-OH cholesterol has no effect on the total phospholipid content but the DPG to PG ratio was markedly decreased. Exchange studies with lipid vesicles revealed that whereas most of the cholesterol underwent exchange, only about 20% of the 7 beta-OH cholesterol was exchanged.

Cardiolipins↗
PubMed1992

The effect of 25-hydroxycholesterol on the regulation of apolipoprotein E mRNA levels and secretion in the human hepatoma HepG2.

The human hepatoma cell line, HepG2, was cultured with 25 OH cholesterol, a potent inhibitor of HMG-CoA reductase, in order to examine the effect of the oxysterol on apo E synthesis and secretion. Treatment of cells with oxysterol (2.5 microM) resulted in a greater than 90% inhibition of HMG-CoA reductase activity and a 3-fold reduction in its cognate mRNA level. However, apo E mRNA level and secretion were not affected after 24 h of drug treatment. This drug treatment was associated with a reduction in both cellular free and esterified cholesterol levels by 50% and 40%, respectively. Exposure of HepG2 cells to an ACAT inhibitor, the Sandoz compound (58-035) for 24 h, at a concentration of 5 micrograms/ml, resulted in a 30% increase and 70% decrease in the intracellular levels of free and esterified cholesterol, respectively. Under this regimen of drug treatment, the level of apo E mRNA was increased by approximately 70%, while HMG-CoA reductase mRNA level was decreased by 35%. When the cells were exposed to the combination of the ACAT inhibitor and 25 OH cholesterol, the cellular levels of free and esterified cholesterol were reduced by 30% and 80%, respectively. This combination of drugs had no effect on apo E mRNA; however, the level of HMG-CoA reductase mRNA was decreased by 3.5-fold. Taken together, the data suggested that reduction in the intracellular levels of either free or esterified cholesterol had no effect on apo E mRNA level. By contrast, a small increment in cellular free cholesterol content was associated with a significant induction in apo E mRNA level. Furthermore, 25 OH cholesterol caused a significant redistribution (50%) of apo E from the HDL fraction to the d greater than 1.21 g/ml infranatant. By using high performance liquid chromatography and molecular sieve columns, it was found that the appearance of a lipid-poor apo E particle was not an artifact of ultracentrifugation. This particle contained 85 wt% protein and 15 wt% of free cholesterol and phospholipid. The results suggested that a lipid-poor apo E particle was secreted by the HepG2 cells under certain circumstances.

Apolipoproteins E↗
PubMed2006

25-Hydroxycholesterol has a dual effect on the proliferation of cultured rat astrocytes.

We examined the effects of 25-OH-cholesterol on the growth of cultured rat astrocytes in the presence of lipoprotein-deficient serum (LPDS). 25-OH-cholesterol at 0.5-8 microM induced an increase in DNA synthesis as measured by [3H]thymidine incorporation into DNA, staining the cells with crystal violet, or counting the number of cells in different phases of the cell cycle by flow cytometry; however, at higher doses, an inhibition of cell proliferation was produced. Similar dose-dependent effects were found in media containing albumin (alone or with added EGF, PDGF, IGF-I or insulin), fetal bovine serum (FBS), or cholesterol-enriched LPDS. Mevalonate, and partially 25-OH-cholesterol, reversed the decrease in cell viability caused by mevinolin (lovastatin). However, mevalonate did not have any effect on 25-OH-cholesterol-stimulated proliferation. Finally, in media with albumin alone or in the presence of fetal bovine serum, growth factors, insulin or forskolin, 25-OH-cholesterol did not affect the expression of either c-fos mRNA or c-fos protein, as measured by real-time quantitative PCR or by Western blot, respectively. These results suggest that 25-OH-cholesterol has a dual effect on the proliferation of cultured rat astrocytes through an AP-1-independent mechanism. This could be of interest for gaining a better knowledge of the pathophysiological processes occurring in these cells.

Animals↗
PubMed1997

25-Hydroxycholesterol causes death but does not prevent nerve growth factor-induced neurite outgrowth in PC12 cells.

The effects of cholesterol oxides on regular and neuronal PC12 cells were examined. Among the cholesterol oxides tested, 7-beta-, 22(R)- and 25-OH-cholesterol were very toxic to regular PC12 cells such that approximately 80% of cells were killed after a 3 day incubation with 20 micrograms/ml (50 microM) of these agents. Cholesterol oxides caused cytotoxicity in neuronal PC12 cells at concentrations higher than those observed for regular PC12 cells. The nerve growth factor (NGF)-induced neurite outgrowth and nitric oxide synthase expression appeared normal in PC12 cells treated with a sublethal dose of 25-OH-cholesterol. Neurite regeneration from established neuronal PC12 cells was not inhibited by the presence of a toxic dose of 25-OH-cholesterol. Given the fact that 25-OH-cholesterol is a potent inhibitor of cholesterol synthesis pathway, these results suggest that the de novo synthesis of cholesterol may not be required for NGF-induced neurite outgrowth in PC12 cells.

Animals↗