Structural Features of Sterols Required to Inhibit Human Sperm Capacitation
Ejaculated mammalian sperm must undergo a final maturation (capacitation) before they can acrosome-react and fertilize eggs. Loss of cholesterol is an essential step in the capacitation of human sperm. Experimentally maintaining a high level of cholesterol inhibits capacitation, but the mechanism is...
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| Veröffentlicht in: | Biology of reproduction 2003-04, Vol.68 (4), p.1308-1317 |
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| creator | NIMMO, Matthew R CROSS, Nicholas L |
| description | Ejaculated mammalian sperm must undergo a final maturation (capacitation) before they can acrosome-react and fertilize eggs.
Loss of cholesterol is an essential step in the capacitation of human sperm. Experimentally maintaining a high level of cholesterol
inhibits capacitation, but the mechanism is unknown. The present study investigated the structural features that are required
for cholesterol's inhibitory activity. Human sperm also contain much desmosterol, which is lost from sperm during capacitation.
Preventing the loss of desmosterol inhibited capacitation (as assessed by acrosomal responsiveness), with an effectiveness
approximately equal to cholesterol's inhibitory activity. Other structural analogs were added to the incubation medium to
replace sperm cholesterol and desmosterol. Most inhibited capacitation, including those that lacked cholesterol's 3β-OH group
(cholesteryl methyl ether and epicholesterol) and those with modified C17 groups (ergosterol and diosgenin). Two steroids
did not inhibit capacitation well. Coprostanol, which has a nonplanar steroid nucleus, had low inhibitory activity that could
be explained by an elevated endogenous cholesterol concentration. Epicoprostanol, which has a nonplanar ring structure and
a 3α-OH group, promoted rather than inhibited capacitation. The inhibitory activity of the analogs was correlated with their
ability to promote order of egg phosphatidylcholine as measured by fluorescence anisotropy. In summary, a planar ring structure
is required for sterol inhibitory activity, but a 3β-OH group and a saturated cholesterol-like aliphatic tail on C17 are not
required. The present results support the hypothesis that sperm sterols block capacitation by increasing order of phospholipids. |
| doi_str_mv | 10.1095/biolreprod.102.008607 |
| format | Article |
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Loss of cholesterol is an essential step in the capacitation of human sperm. Experimentally maintaining a high level of cholesterol
inhibits capacitation, but the mechanism is unknown. The present study investigated the structural features that are required
for cholesterol's inhibitory activity. Human sperm also contain much desmosterol, which is lost from sperm during capacitation.
Preventing the loss of desmosterol inhibited capacitation (as assessed by acrosomal responsiveness), with an effectiveness
approximately equal to cholesterol's inhibitory activity. Other structural analogs were added to the incubation medium to
replace sperm cholesterol and desmosterol. Most inhibited capacitation, including those that lacked cholesterol's 3β-OH group
(cholesteryl methyl ether and epicholesterol) and those with modified C17 groups (ergosterol and diosgenin). Two steroids
did not inhibit capacitation well. Coprostanol, which has a nonplanar steroid nucleus, had low inhibitory activity that could
be explained by an elevated endogenous cholesterol concentration. Epicoprostanol, which has a nonplanar ring structure and
a 3α-OH group, promoted rather than inhibited capacitation. The inhibitory activity of the analogs was correlated with their
ability to promote order of egg phosphatidylcholine as measured by fluorescence anisotropy. In summary, a planar ring structure
is required for sterol inhibitory activity, but a 3β-OH group and a saturated cholesterol-like aliphatic tail on C17 are not
required. The present results support the hypothesis that sperm sterols block capacitation by increasing order of phospholipids.</description><identifier>ISSN: 0006-3363</identifier><identifier>EISSN: 1529-7268</identifier><identifier>DOI: 10.1095/biolreprod.102.008607</identifier><identifier>PMID: 12606419</identifier><identifier>CODEN: BIREBV</identifier><language>eng</language><publisher>Madison, WI: Society for the Study of Reproduction</publisher><subject>Biological and medical sciences ; Cholestanol - pharmacology ; Cholesterol - pharmacology ; Desmosterol - pharmacology ; Fundamental and applied biological sciences. Psychology ; Humans ; Male ; Mammalian male genital system ; Molecular Conformation ; Morphology. Physiology ; Sperm Capacitation - drug effects ; Stereoisomerism ; Sterols - chemistry ; Sterols - pharmacology ; Vertebrates: reproduction</subject><ispartof>Biology of reproduction, 2003-04, Vol.68 (4), p.1308-1317</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15077153$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12606419$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NIMMO, Matthew R</creatorcontrib><creatorcontrib>CROSS, Nicholas L</creatorcontrib><title>Structural Features of Sterols Required to Inhibit Human Sperm Capacitation</title><title>Biology of reproduction</title><addtitle>Biol Reprod</addtitle><description>Ejaculated mammalian sperm must undergo a final maturation (capacitation) before they can acrosome-react and fertilize eggs.
Loss of cholesterol is an essential step in the capacitation of human sperm. Experimentally maintaining a high level of cholesterol
inhibits capacitation, but the mechanism is unknown. The present study investigated the structural features that are required
for cholesterol's inhibitory activity. Human sperm also contain much desmosterol, which is lost from sperm during capacitation.
Preventing the loss of desmosterol inhibited capacitation (as assessed by acrosomal responsiveness), with an effectiveness
approximately equal to cholesterol's inhibitory activity. Other structural analogs were added to the incubation medium to
replace sperm cholesterol and desmosterol. Most inhibited capacitation, including those that lacked cholesterol's 3β-OH group
(cholesteryl methyl ether and epicholesterol) and those with modified C17 groups (ergosterol and diosgenin). Two steroids
did not inhibit capacitation well. Coprostanol, which has a nonplanar steroid nucleus, had low inhibitory activity that could
be explained by an elevated endogenous cholesterol concentration. Epicoprostanol, which has a nonplanar ring structure and
a 3α-OH group, promoted rather than inhibited capacitation. The inhibitory activity of the analogs was correlated with their
ability to promote order of egg phosphatidylcholine as measured by fluorescence anisotropy. In summary, a planar ring structure
is required for sterol inhibitory activity, but a 3β-OH group and a saturated cholesterol-like aliphatic tail on C17 are not
required. The present results support the hypothesis that sperm sterols block capacitation by increasing order of phospholipids.</description><subject>Biological and medical sciences</subject><subject>Cholestanol - pharmacology</subject><subject>Cholesterol - pharmacology</subject><subject>Desmosterol - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Male</subject><subject>Mammalian male genital system</subject><subject>Molecular Conformation</subject><subject>Morphology. Physiology</subject><subject>Sperm Capacitation - drug effects</subject><subject>Stereoisomerism</subject><subject>Sterols - chemistry</subject><subject>Sterols - pharmacology</subject><subject>Vertebrates: reproduction</subject><issn>0006-3363</issn><issn>1529-7268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkNFLwzAQxoMobk7_BCUv-la9JG3aPspwThwITp_LLU1cJG1nkjL87w048enuuB_ffd8RcsnglkFd3G3s4Lze-aFNM78FqCSUR2TKCl5nJZfVMZkCgMyEkGJCzkL4BGC54OKUTBiXIHNWT8nzOvpRxdGjowuNqdGBDoauo_aDC_RVf43W65bGgT71W7uxkS7HDnu63mnf0TnuUNmI0Q79OTkx6IK-ONQZeV88vM2X2erl8Wl-v8q2yUrMWsmUxpJvBKLCFo0BCUaAFIqnheFSlbKqpeFa5ZALo1mR6wKgrURdAIoZufnVTem_Rh1i09mgtHPY62EMTSkY5zXjCbw6gOOm022z87ZD_938xU_A9QHAoNAZj72y4Z8roCxZIf4vbu3Hdp_-0YQOnUuyotnv97Jq8oYJqMQPxAB54A</recordid><startdate>20030401</startdate><enddate>20030401</enddate><creator>NIMMO, Matthew R</creator><creator>CROSS, Nicholas L</creator><general>Society for the Study of Reproduction</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20030401</creationdate><title>Structural Features of Sterols Required to Inhibit Human Sperm Capacitation</title><author>NIMMO, Matthew R ; CROSS, Nicholas L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h363t-d61cea72b3aacadaff060f3063c2ceaf26c76896f2ec4043fe154e500d83950a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Biological and medical sciences</topic><topic>Cholestanol - pharmacology</topic><topic>Cholesterol - pharmacology</topic><topic>Desmosterol - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Male</topic><topic>Mammalian male genital system</topic><topic>Molecular Conformation</topic><topic>Morphology. Physiology</topic><topic>Sperm Capacitation - drug effects</topic><topic>Stereoisomerism</topic><topic>Sterols - chemistry</topic><topic>Sterols - pharmacology</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NIMMO, Matthew R</creatorcontrib><creatorcontrib>CROSS, Nicholas L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Biology of reproduction</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NIMMO, Matthew R</au><au>CROSS, Nicholas L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Structural Features of Sterols Required to Inhibit Human Sperm Capacitation</atitle><jtitle>Biology of reproduction</jtitle><addtitle>Biol Reprod</addtitle><date>2003-04-01</date><risdate>2003</risdate><volume>68</volume><issue>4</issue><spage>1308</spage><epage>1317</epage><pages>1308-1317</pages><issn>0006-3363</issn><eissn>1529-7268</eissn><coden>BIREBV</coden><abstract>Ejaculated mammalian sperm must undergo a final maturation (capacitation) before they can acrosome-react and fertilize eggs.
Loss of cholesterol is an essential step in the capacitation of human sperm. Experimentally maintaining a high level of cholesterol
inhibits capacitation, but the mechanism is unknown. The present study investigated the structural features that are required
for cholesterol's inhibitory activity. Human sperm also contain much desmosterol, which is lost from sperm during capacitation.
Preventing the loss of desmosterol inhibited capacitation (as assessed by acrosomal responsiveness), with an effectiveness
approximately equal to cholesterol's inhibitory activity. Other structural analogs were added to the incubation medium to
replace sperm cholesterol and desmosterol. Most inhibited capacitation, including those that lacked cholesterol's 3β-OH group
(cholesteryl methyl ether and epicholesterol) and those with modified C17 groups (ergosterol and diosgenin). Two steroids
did not inhibit capacitation well. Coprostanol, which has a nonplanar steroid nucleus, had low inhibitory activity that could
be explained by an elevated endogenous cholesterol concentration. Epicoprostanol, which has a nonplanar ring structure and
a 3α-OH group, promoted rather than inhibited capacitation. The inhibitory activity of the analogs was correlated with their
ability to promote order of egg phosphatidylcholine as measured by fluorescence anisotropy. In summary, a planar ring structure
is required for sterol inhibitory activity, but a 3β-OH group and a saturated cholesterol-like aliphatic tail on C17 are not
required. The present results support the hypothesis that sperm sterols block capacitation by increasing order of phospholipids.</abstract><cop>Madison, WI</cop><pub>Society for the Study of Reproduction</pub><pmid>12606419</pmid><doi>10.1095/biolreprod.102.008607</doi><tpages>10</tpages></addata></record> |
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| ispartof | Biology of reproduction, 2003-04, Vol.68 (4), p.1308-1317 |
| issn | 0006-3363 1529-7268 |
| language | eng |
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| source | MEDLINE; BioOne Complete; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals |
| subjects | Biological and medical sciences Cholestanol - pharmacology Cholesterol - pharmacology Desmosterol - pharmacology Fundamental and applied biological sciences. Psychology Humans Male Mammalian male genital system Molecular Conformation Morphology. Physiology Sperm Capacitation - drug effects Stereoisomerism Sterols - chemistry Sterols - pharmacology Vertebrates: reproduction |
| title | Structural Features of Sterols Required to Inhibit Human Sperm Capacitation |
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