Cholesterol is the principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
Cholesterol is biosynthesized by all animal cells and is an essential structural and signaling component of animal cell membranes. In vertebrates, hepatic cells typically produce the greatest amounts. In the brain, astrocytes produce cholesterol and transport it to neurons. It is absent among prokaryotes (bacteria and archaea), although there are some exceptions, such as Mycoplasma, which require cholesterol for growth. Cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acid and vitamin D.
Elevated levels of cholesterol in the blood, especially when bound to low-density lipoprotein (LDL, often referred to as "bad cholesterol"), may increase the risk of cardiovascular disease.
François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. In 1815, chemist Michel Eugène Chevreul named the compound "cholesterine". |
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InChI=1S/C27H46O/c1-18(2)7-6-8-19(3)23-11-12-24-22-10-9-20-17-21(28)13-15-26(20,4)25(22)14-16-27(23,24)5/h9,18-19,21-25,28H,6-8,10-17H2,1-5H3/t19-,21+,22+,23-,24+,25+,26+,27-/m1/s1 |
HVYWMOMLDIMFJA-DPAQBDIFSA-N |
C1[C@@]2([C@]3(CC[C@]4([C@]([C@@]3(CC=C2C[C@H](C1)O)[H])(CC[C@@]4([C@H](C)CCCC(C)C)[H])[H])C)[H])C |
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Mus musculus
(NCBI:txid10090)
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See:
PubMed
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Mus musculus
(NCBI:txid10090)
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Source: BioModels - MODEL1507180067
See:
PubMed
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Daphnia galeata
(NCBI:txid27404)
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See:
PubMed
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Chlamydomonas reinhardtii
(NCBI:txid3055)
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See:
PubMed
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
algal metabolite
Any eukaryotic metabolite produced during a metabolic reaction in algae including unicellular organisms like chlorella and diatoms to multicellular organisms like giant kelps and brown algae.
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
Daphnia galeata metabolite
A Daphnia metabolite produced by the species Daphnia galeata.
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View more via ChEBI Ontology
Outgoing
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cholesterol
(CHEBI:16113)
has role
Daphnia galeata metabolite
(CHEBI:83038)
cholesterol
(CHEBI:16113)
has role
algal metabolite
(CHEBI:84735)
cholesterol
(CHEBI:16113)
has role
human metabolite
(CHEBI:77746)
cholesterol
(CHEBI:16113)
has role
mouse metabolite
(CHEBI:75771)
cholesterol
(CHEBI:16113)
is a
3β-hydroxy-Δ5-steroid
(CHEBI:1722)
cholesterol
(CHEBI:16113)
is a
3β-sterol
(CHEBI:35348)
cholesterol
(CHEBI:16113)
is a
C27-steroid
(CHEBI:131619)
cholesterol
(CHEBI:16113)
is a
cholestanoid
(CHEBI:50401)
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Incoming
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(16S,22S)-dihydroxycholesterol
(CHEBI:191938)
has functional parent
cholesterol
(CHEBI:16113)
(20R)-17α,20-dihydroxycholesterol
(CHEBI:783)
has functional parent
cholesterol
(CHEBI:16113)
(20S)-17α,20-dihydroxycholesterol
(CHEBI:182953)
has functional parent
cholesterol
(CHEBI:16113)
(22R)-22-hydroxycholesterol
(CHEBI:67237)
has functional parent
cholesterol
(CHEBI:16113)
(22S)-22-hydroxycholesterol
(CHEBI:1301)
has functional parent
cholesterol
(CHEBI:16113)
(24S,25)-dihydroxycholesterol
(CHEBI:86074)
has functional parent
cholesterol
(CHEBI:16113)
(24S,26)-dihydroxycholesterol
(CHEBI:86075)
has functional parent
cholesterol
(CHEBI:16113)
(25R)-3β,26-dihydroxycholest-5-en-7-one
(CHEBI:87653)
has functional parent
cholesterol
(CHEBI:16113)
(25R)-3β-hydroxycholest-5-en-7-one-26-al
(CHEBI:87677)
has functional parent
cholesterol
(CHEBI:16113)
(25R)-3β-hydroxycholest-5-en-7-one-26-oic acid
(CHEBI:87783)
has functional parent
cholesterol
(CHEBI:16113)
(25R)-cholest-5-ene-3β,26-diol
(CHEBI:76591)
has functional parent
cholesterol
(CHEBI:16113)
24-hydroxycholesterol
(CHEBI:50515)
has functional parent
cholesterol
(CHEBI:16113)
24-methylenecholesterol
(CHEBI:19812)
has functional parent
cholesterol
(CHEBI:16113)
25-hydroxycholesterol
(CHEBI:42977)
has functional parent
cholesterol
(CHEBI:16113)
26-hydroxycholesterol
(CHEBI:17703)
has functional parent
cholesterol
(CHEBI:16113)
3β-hydroxycholest-5-en-26-al
(CHEBI:84145)
has functional parent
cholesterol
(CHEBI:16113)
3β-hydroxycholest-5-en-26-oic acid
(CHEBI:81014)
has functional parent
cholesterol
(CHEBI:16113)
4β-hydroxycholesterol
(CHEBI:85778)
has functional parent
cholesterol
(CHEBI:16113)
7α,24-dihydroxycholesterol
(CHEBI:50517)
has functional parent
cholesterol
(CHEBI:16113)
7α,25-dihydroxycholesterol
(CHEBI:37623)
has functional parent
cholesterol
(CHEBI:16113)
7α,26-dihydroxycholesterol
(CHEBI:18431)
has functional parent
cholesterol
(CHEBI:16113)
7α-hydroxycholesterol
(CHEBI:17500)
has functional parent
cholesterol
(CHEBI:16113)
7β-hydroxycholesterol
(CHEBI:42989)
has functional parent
cholesterol
(CHEBI:16113)
7-aminocholesterol
(CHEBI:77845)
has functional parent
cholesterol
(CHEBI:16113)
7-ketocholesterol
(CHEBI:64294)
has functional parent
cholesterol
(CHEBI:16113)
cholesterol sulfate
(CHEBI:41321)
has functional parent
cholesterol
(CHEBI:16113)
cholesteryl β-D-glucoside
(CHEBI:17495)
has functional parent
cholesterol
(CHEBI:16113)
cholesteryl ester
(CHEBI:17002)
has functional parent
cholesterol
(CHEBI:16113)
cholesteryl glycoside
(CHEBI:61656)
has functional parent
cholesterol
(CHEBI:16113)
cholesteryl hemisuccinate
(CHEBI:138742)
has functional parent
cholesterol
(CHEBI:16113)
Glycino 3β-cholesterol ester group
(CHEBI:143135)
has functional parent
cholesterol
(CHEBI:16113)
oxysterol
(CHEBI:53030)
has functional parent
cholesterol
(CHEBI:16113)
cholesteryl β-D-galactoside
(CHEBI:189066)
has part
cholesterol
(CHEBI:16113)
cholesteryl β-D-xyloside
(CHEBI:189067)
has part
cholesterol
(CHEBI:16113)
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(3β,14β,17α)-cholest-5-en-3-ol
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IUPAC
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Cholest-5-en-3beta-ol
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KEGG COMPOUND
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Cholesterin
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NIST Chemistry WebBook
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Cholesterol
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KEGG COMPOUND
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CHOLESTEROL
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PDBeChem
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cholesterol
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UniProt
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2060565
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Reaxys Registry Number
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Reaxys
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550297
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Gmelin Registry Number
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Gmelin
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57-88-5
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CAS Registry Number
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KEGG COMPOUND
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57-88-5
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CAS Registry Number
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ChemIDplus
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57-88-5
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CAS Registry Number
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NIST Chemistry WebBook
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Morzycki JW, Sobkowiak A (2015) Electrochemical oxidation of cholesterol. Beilstein journal of organic chemistry 11, 392-402 [PubMed:25977713] [show Abstract] Indirect cholesterol electrochemical oxidation in the presence of various mediators leads to electrophilic addition to the double bond, oxidation at the allylic position, oxidation of the hydroxy group, or functionalization of the side chain. Recent studies have proven that direct electrochemical oxidation of cholesterol is also possible and affords different products depending on the reaction conditions. | Levinson SS, Wagner SG (2015) Implications of reverse cholesterol transport: recent studies. Clinica chimica acta; international journal of clinical chemistry 439, 154-161 [PubMed:25451949] [show Abstract]
IntroductionThere is a strong epidemiological relationship between high density lipoproteins and atherosclerotic coronary vascular disease (ASCVD). The process of reverse cholesterol transport (RCT) has been hypothesized to help explain this relationship. The corollary that raising HDL should reduce ASCVD is also drawn from this relationship. In recent years, the metabolism of HDL has become better understood. A hypothetical process for explaining RCT has been superimposed on the currently understood HDL metabolic pathways.MethodsOutline of HDL metabolism and the superimposed RCT process. Literature review of studies of persons with genetic defects, HDL cholesterol raising clinical trials, Mendelian randomization studies and treatments with molecules that mimic HDL.ConclusionsMutation studies of ABCA1, LCAT and SR-B1 genes in humans showed expected variations in HDLC but little association with ASCVD and there was no significant association between HDLC and ASCVD in Mendelian randomization studies. Elevations in HDLC due to treatment with niacin and cholesteryl ester transport protein inhibitors in randomized trials raised HDLC but did not significantly reduce risk of ASCVD. Treatment with molecules that mimic HDL did not seem to reduce ASCVD. Thus, recent evidence does not seem to support RCT as currently proposed. This hypothesis seems to need substantial revision. | Iaea DB, Maxfield FR (2015) Cholesterol trafficking and distribution. Essays in biochemistry 57, 43-55 [PubMed:25658343] [show Abstract] Sterols are a critical component of cell membranes of eukaryotes. In mammalian cells there is approximately a six-fold range in the cholesterol content in various organelles. The cholesterol content of membranes plays an important role in organizing membranes for signal transduction and protein trafficking as well as in modulating the physiochemical properties of membranes. Cholesterol trafficking among organelles is highly dynamic and is mediated by both vesicular and non-vesicular processes. Several proteins have been proposed to mediate inter-organelle trafficking of cholesterol. However, several aspects of the mechanisms involved in regulating trafficking and distribution of cholesterol remain to be elucidated. In the present chapter, we discuss the cellular mechanisms involved in cholesterol distribution and the trafficking processes involved in maintaining sterol homoeostasis. | Derewiaka D, Molińska née Sosińska E (2015) Cholesterol transformations during heat treatment. Food chemistry 171, 233-240 [PubMed:25308664] [show Abstract] The aim of the study was to characterise products of cholesterol standard changes during thermal processing. Cholesterol was heated at 120°C, 150°C, 180°C and 220°C from 30 to 180 min. The highest losses of cholesterol content were found during thermal processing at 220°C, whereas the highest content of cholesterol oxidation products was observed at temperature of 150°C. The production of volatile compounds was stimulated by the increase of temperature. Treatment of cholesterol at higher temperatures i.e. 180°C and 220°C led to the formation of polymers and other products e.g. cholestadienes and fragmented cholesterol molecules. Further studies are required to identify the structure of cholesterol oligomers and to establish volatile compounds, which are markers of cholesterol transformations, mainly oxidation. | Favari E, Chroni A, Tietge UJ, Zanotti I, Escolà-Gil JC, Bernini F (2015) Cholesterol efflux and reverse cholesterol transport. Handbook of experimental pharmacology 224, 181-206 [PubMed:25522988] [show Abstract] Both alterations of lipid/lipoprotein metabolism and inflammatory events contribute to the formation of the atherosclerotic plaque, characterized by the accumulation of abnormal amounts of cholesterol and macrophages in the artery wall. Reverse cholesterol transport (RCT) may counteract the pathogenic events leading to the formation and development of atheroma, by promoting the high-density lipoprotein (HDL)-mediated removal of cholesterol from the artery wall. Recent in vivo studies established the inverse relationship between RCT efficiency and atherosclerotic cardiovascular diseases (CVD), thus suggesting that the promotion of this process may represent a novel strategy to reduce atherosclerotic plaque burden and subsequent cardiovascular events. HDL plays a primary role in all stages of RCT: (1) cholesterol efflux, where these lipoproteins remove excess cholesterol from cells; (2) lipoprotein remodeling, where HDL undergo structural modifications with possible impact on their function; and (3) hepatic lipid uptake, where HDL releases cholesterol to the liver, for the final excretion into bile and feces. Although the inverse association between HDL plasma levels and CVD risk has been postulated for years, recently this concept has been challenged by studies reporting that HDL antiatherogenic functions may be independent of their plasma levels. Therefore, assessment of HDL function, evaluated as the capacity to promote cell cholesterol efflux may offer a better prediction of CVD than HDL levels alone. Consistent with this idea, it has been recently demonstrated that the evaluation of serum cholesterol efflux capacity (CEC) is a predictor of atherosclerosis extent in humans. | Varbo A, Benn M, Nordestgaard BG (2014) Remnant cholesterol as a cause of ischemic heart disease: evidence, definition, measurement, atherogenicity, high risk patients, and present and future treatment. Pharmacology & therapeutics 141, 358-367 [PubMed:24287311] [show Abstract] This review focuses on remnant cholesterol as a causal risk factor for ischemic heart disease (IHD), on its definition, measurement, atherogenicity, and levels in high risk patient groups; in addition, present and future pharmacological approaches to lowering remnant cholesterol levels are considered. Observational studies show association between elevated levels of remnant cholesterol and increased risk of cardiovascular disease, even when remnant cholesterol levels are defined, measured, or calculated in different ways. In-vitro and animal studies also support the contention that elevated levels of remnant cholesterol may cause atherosclerosis same way as elevated levels of low-density lipoprotein (LDL) cholesterol, by cholesterol accumulation in the arterial wall. Genetic studies of variants associated with elevated remnant cholesterol levels show that an increment of 1mmol/L (39mg/dL) in levels of nonfasting remnant cholesterol associates with a 2.8-fold increased risk of IHD, independently of high-density lipoprotein cholesterol levels. Results from genetic studies also show that elevated levels of remnant cholesterol are causally associated with both low-grade inflammation and IHD. However, elevated levels of LDL cholesterol are associated with IHD, but not with low-grade inflammation. Such results indicate that elevated LDL cholesterol levels cause atherosclerosis without a major inflammatory component, whereas an inflammatory component of atherosclerosis is driven by elevated remnant cholesterol levels. Post-hoc subgroup analyses of randomized trials using fibrates in individuals with elevated triglyceride levels, elevated remnant cholesterol levels, show a benefit of lowering triglycerides or remnant cholesterol levels; however, large randomized trials with the primary target of lowering remnant cholesterol levels are still missing. | Kanter JL, Narayana S, Ho PP, Catz I, Warren KG, Sobel RA, Steinman L, Robinson WH (2006) Lipid microarrays identify key mediators of autoimmune brain inflammation. Nature medicine 12, 138-143 [PubMed:16341241] [show Abstract] Recent studies suggest that increased T-cell and autoantibody reactivity to lipids may be present in the autoimmune demyelinating disease multiple sclerosis. To perform large-scale multiplex analysis of antibody responses to lipids in multiple sclerosis, we developed microarrays composed of lipids present in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain lipid fractions. Lipid-array analysis showed lipid-specific antibodies against sulfatide, sphingomyelin and oxidized lipids in cerebrospinal fluid (CSF) derived from individuals with multiple sclerosis. Sulfatide-specific antibodies were also detected in SJL/J mice with acute experimental autoimmune encephalomyelitis (EAE). Immunization of mice with sulfatide plus myelin peptide resulted in a more severe disease course of EAE, and administration of sulfatide-specific antibody exacerbated EAE. Thus, autoimmune responses to sulfatide and other lipids are present in individuals with multiple sclerosis and in EAE, and may contribute to the pathogenesis of autoimmune demyelination. | Haines TH (2001) Do sterols reduce proton and sodium leaks through lipid bilayers? Progress in lipid research 40, 299-324 [PubMed:11412894] [show Abstract] Proton and/or sodium electrochemical gradients are critical to energy handling at the plasma membranes of all living cells. Sodium gradients are used for animal plasma membranes, all other living organisms use proton gradients. These chemical and electrical gradients are either created by a cation pumping ATPase or are created by photons or redox, used to make ATP. It has been established that both hydrogen and sodium ions leak through lipid bilayers at approximately the same rate at the concentration they occur in living organisms. Although the gradients are achieved by pumping the cations out of the cell, the plasma membrane potential enhances the leakage rate of these cations into the cell because of the orientation of the potential. This review proposes that cells use certain lipids to inhibit cation leakage through the membrane bilayers. It assumes that Na(+) leaks through the bilayer by a defect mechanism. For Na(+) leakage in animal plasma membranes, the evidence suggests that cholesterol is a key inhibitor of Na(+) leakage. Here I put forth a novel mechanism for proton leakage through lipid bilayers. The mechanism assumes water forms protonated and deprotonated clusters in the lipid bilayer. The model suggests how two features of lipid structures may inhibit H(+) leakage. One feature is the fused ring structure of sterols, hopanoids and tetrahymenol which extrude water and therefore clusters from the bilayer. The second feature is lipid structures that crowd the center of the bilayer with hydrocarbon. This can be accomplished either by separating the two monolayers with hydrocarbons such as isoprenes or isopranes in the bilayer's cleavage plane or by branching the lipid chains in the center of the bilayers with hydrocarbon. The natural distribution of lipids that contain these features are examined. Data in the literature shows that plasma membranes exposed to extreme concentrations of cations are particularly rich in the lipids containing the predicted qualities. Prokaryote plasma membranes that reside in extreme acids (acidophiles) contain both hopanoids and iso/anteiso- terminal lipid branching. Plasma membranes that reside in extreme base (alkaliphiles) contain both squalene and iso/anteiso- lipids. The mole fraction of squalene in alkaliphile bilayers increases, as they are cultured at higher pH. In eukaryotes, cation leak inhibition is here attributed to sterols and certain isoprenes, dolichol for lysosomes and peroxysomes, ubiquinone for these in addition to mitochondrion, and plastoquinone for the chloroplast. Phytosterols differ from cholesterol because they contain methyl and ethyl branches on the side chain. The proposal provides a structure-function rationale for distinguishing the structures of the phytosterols as inhibitors of proton leaks from that of cholesterol which is proposed to inhibit leaks of Na(+). The most extensively studied of sterols, cholesterol, occurs only in animal cells where there is a sodium gradient across the plasma membrane. In mammals, nearly 100 proteins participate in cholesterol's biosynthetic and degradation pathway, its regulatory mechanisms and cell-delivery system. Although a fat, cholesterol yields no energy on degradation. Experiments have shown that it reduces Na(+) and K(+) leakage through lipid bilayers to approximately one third of bilayers that lack the sterol. If sterols significantly inhibit cation leakage through the lipids of the plasma membrane, then the general role of all sterols is to save metabolic ATP energy, which is the penalty for cation leaks into the cytosol. The regulation of cholesterol's appearance in the plasma membrane and the evolution of sterols is discussed in light of this proposed role. | Motamed Khorasani A, Cheung AP, Lee CY (2000) Cholesterol inhibitory effects on human sperm-induced acrosome reaction. Journal of andrology 21, 586-594 [PubMed:10901445] [show Abstract] Progesterone (P4) is known to induce an acrosome reaction in mammalian sperm in vitro, whereas cholesterol is a major inhibitor of acrosome reaction. This study had three objectives: to study the in vitro effects of exogenous cholesterol on acrosome reactions in human sperm, to study the mechanism by which cholesterol affects P4-induced acrosome reaction and those induced by dibutyryl cyclic adenosine monophosphate (db-cAMP), and to study the status of the P4 surface receptor during capacitation and acrosome reaction and its relationship with cholesterol and different acrosome reaction inducers. Acrosome reaction was induced with exposure to 10 microg/mL of P4 for 30 minutes and 1 mM of db-cAMP for 30 minutes in motile sperm either in the presence or absence of 0.1-1 microg/mL of cholesterol for 30 minutes. The effects of a 30-minute exposure to 1 microg/mL of beta-sitosterol, a cholesterol plant analogue, as well as the effects of cholesterol on P4-induced acrosome reactions were compared. Fluorescein isothiocyanate-labeled albumin-progesterone conjugate (P4-FITC-BSA) was used as the probe in order to quantify the percentage of sperm in which the P, surface receptor was exposed. The results of this study indicate that cholesterol inhibited P4-induced acrosome reactions when added to the sperm during capacitation (long incubation) and when it was added with P4 during the induction of acrosome reactions (short incubation). Similarly, acrosome reaction that was induced by db-cAMP was also inhibited by cholesterol. Fifty percent of P4-induced acrosome reaction was inhibited by a cholesterol concentration of 0.2 microg/mL. Cholesterol's inhibition of induced acrosome reaction was independent of P4 concentration. Beta-sitosterol inhibited P4-induced acrosome reaction in a dose-dependent manner that was identical to that of cholesterol. We observed that increases in the P4 surface receptor exposure were time-dependent and receptors migrated toward the equatorial segment during the first 2 hours of capacitation. We also found that db-cAMP induced the appearance of the P4 surface receptor in the sperm plasma membrane and that cholesterol inhibited it. The results of this study suggest that cholesterol inhibits acrosome reaction in a noncompetitive manner by modifying the structure of the sperm plasma membrane, which prevents exposure of the P4 surface receptor for P4 binding. | Cross NL (1996) Human seminal plasma prevents sperm from becoming acrosomally responsive to the agonist, progesterone: cholesterol is the major inhibitor. Biology of reproduction 54, 138-145 [PubMed:8838010] [show Abstract] Seminal plasma inhibits human sperm from developing the ability to undergo the acrosome reaction. The inhibitory activity was identified as that of cholesterol on the basis of its solubility in organic solvents, its chromatographic behavior (adsorption, thin-layer, and gas chromatography), and its mass spectrum. Contrary to findings in other reports, no evidence for inhibitory proteins or peptides was found, and spermine was not an effective inhibitor. The inhibitory activity of untreated seminal plasma from individual ejaculates was highly correlated with the cholesterol content of the ejaculates (r = 0.96), suggesting that the amount of cholesterol determines the inhibitory activity of unfractionated seminal plasma. The inhibitory activity of unfractionated seminal plasma was significantly less, relative to the cholesterol content, than the activity of pure cholesterol, which is consistent with the idea that there are components in seminal plasma that partially counter the effect of cholesterol by promoting the development of acrosomal responsiveness. | Weibust RS (1973) Inheritance of plasma cholesterol levels in mice. Genetics 73, 303-312 [PubMed:4696527] [show Abstract] Mean plasma cholesterol levels were determined at two ages in mice from eight unrelated inbred strains (BALB/cJ, BDP/J, CBA/J, C57BL/6J, LP/J, RF/J, SJL/J, and 129/J). Significant strain, sex, and age differences were observed. Estimates of the degree of genetic determination of the trait obtained from an analysis of the strain data averaged 58 +/- 4% for the males and 54 +/- 8% for the females.-Selection for high and low plasma cholesterol levels produced two significantly different and distinct lines. Selection was initiated in a genetically heterogeneous population derived from an eight-way cross of the inbred strains listed above. After five generations of selection the divergence of the high and low lines amounted to 4 phenotypic standard deviations of the foundation population. Realized heritability estimated from the regression of divergence on the combined cumulative selection differential was 51 +/- 5% for the males and 50 +/- 3% for the females. The results indicate that genetic factors are important in controlling plasma cholesterol levels in the mouse and that the majority of these factors act additively. |
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