Estrogen: Béda antara owahan
| Larik 16: | Larik 16: | ||
| title = UGT1A1 Genetic Polymorphisms, Endogenous Estrogen Exposure, Soy Food Intake, and Endometrial Cancer Risk |
| title = UGT1A1 Genetic Polymorphisms, Endogenous Estrogen Exposure, Soy Food Intake, and Endometrial Cancer Risk |
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| work = Vanderbilt Epidemiology Center, Department of Medicine and Vanderbilt-Ingram Cancer Center, Nashville, Tennessee and Department of Epidemiology, Shanghai Cancer Institute, Cancer Institute of Shanghai Jiao Tong University; Sandra L. Deming, Wei Zheng, Wang-Hong Xu, Qiuyin Cai, Zhixian Ruan, Yong-Bing Xiang dan Xiao-Ou Shu |
| work = Vanderbilt Epidemiology Center, Department of Medicine and Vanderbilt-Ingram Cancer Center, Nashville, Tennessee and Department of Epidemiology, Shanghai Cancer Institute, Cancer Institute of Shanghai Jiao Tong University; Sandra L. Deming, Wei Zheng, Wang-Hong Xu, Qiuyin Cai, Zhixian Ruan, Yong-Bing Xiang dan Xiao-Ou Shu |
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}}(Kaunduh 30/1/13)</ref> Mekanisme klasik estrogen bakal duweni pengaruh tumprap laju dalan [[mitosis]] lan [[apoptosis]] lan ngejawantah dadi risiko kanker payudara kanti ngaruhi pertumbuhan [[sel epitelial|jaringan epitelial]]. Laju [[proliferasi]] [[sel (biologi)|sel]] kang cepet banget bakal gawé sel dadi rentan tumprap kesalahan [[gen]]etika nalika proses [[replikasi DNA]] |
}}(Kaunduh 30/1/13)</ref> Mekanisme klasik estrogen bakal duweni pengaruh tumprap laju dalan [[mitosis]] lan [[apoptosis]] lan ngejawantah dadi risiko kanker payudara kanti ngaruhi pertumbuhan [[sel epitelial|jaringan epitelial]]. Laju [[proliferasi]] [[sel (biologi)|sel]] kang cepet banget bakal gawé sel dadi rentan tumprap kesalahan [[gen]]etika nalika proses [[replikasi DNA]] déning senyawa [[spesi oksigen reaktif]] kang teraktivasi déning [[metabolit]] estrogen. Senajan mengkono, fitoestrogen isa mudunake risiko kasebut kanti kapasitase berkompetisi karo estrogen ing pencerape, sahingga menstimulasi produksi [[globulin]] pengusung hormon seks lan ngalonake aktvitas enzim ing lintasa sintesis estrogen. |
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Nalika ngalami [[katabolisme]], estrogen bakal mbentuk pira-pira senyawa [[intermediat]] kang disebut estrogen-[[katekol]] lewati 2 [[lintasan metabolisme|lintasan]] ''2-hydroxylation'' karo enzim [[CYP1A1]] lan ''4-hydroxylation'' karo enzim [[CYP1B1]],<ref>{{en}}{{cite web |
Nalika ngalami [[katabolisme]], estrogen bakal mbentuk pira-pira senyawa [[intermediat]] kang disebut estrogen-[[katekol]] lewati 2 [[lintasan metabolisme|lintasan]] ''2-hydroxylation'' karo enzim [[CYP1A1]] lan ''4-hydroxylation'' karo enzim [[CYP1B1]],<ref>{{en}}{{cite web |
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Révisi kala 2 Maret 2016 09.19
Estrogen (-utawa oestrogen) -ya iku sekelompok senyawa steroid kang fungsine utamane minangka hormon seks wanita. Senajan turah isa iku ing jero awak pria utawa wanita, kandungane luwih duwur ing awak wanita umur subur. Hormon iki nyebapake perkembangan lan nahanake tanda-tanda kelamin sekunder ing wanita, kaya susu, lan uga melu sajrone kekandelan endometrium utawa sajrone pengaturan siklus haid. nalika wektu menopause, estrogen mulai kurang sahingga isa nyebapake pira-pira efek, ing antarane hot flash, kanti kringet nalika wektu turu, lan was-was kang ora wajar.
telu jenis estrogen utama kang turah sacara alami sajrone awak wanita ya iku estradiol, estriol, lan estron. Awit menarche nganti menopause, estrogen utama -ya iku 17β-estradiol. Ing jero awak, katelu jenis estrogen kasebut digawé saka androgen kanti bantuan enzim. Estradiol digawé saka testosteron, wondene estron digawé saka androstenadion. Estron kanti sifat luwih lemah ketimbang estradiol, lan ing wanita pasca menopause estron ditemokake luwih akeh ketimbang estradiol. Pira-pira zat alami utawa gawéyan wis ditemokake duweni aktivitas kang sifate pada estrogen[1]. Zat gawéyan kang sifate kaya estrogen disebut xenoestrogen, wondene bahan alami saka wit-witan kang duweni aktivitas kaya estrogen disebut fitoestrogen.
Estrogen digunakake minangka bahan pil kontrasepsi lan juga terapi kanggo wanita menopause.
Terpapar hormon estrogen kanti ura aturan lan kumulatif, dianggep isa ningkatke risiko kena kanker payudara,[2] lan kanker endometrium.[3] Mekanisme klasik estrogen bakal duweni pengaruh tumprap laju dalan mitosis lan apoptosis lan ngejawantah dadi risiko kanker payudara kanti ngaruhi pertumbuhan jaringan epitelial. Laju proliferasi sel kang cepet banget bakal gawé sel dadi rentan tumprap kesalahan genetika nalika proses replikasi DNA déning senyawa spesi oksigen reaktif kang teraktivasi déning metabolit estrogen. Senajan mengkono, fitoestrogen isa mudunake risiko kasebut kanti kapasitase berkompetisi karo estrogen ing pencerape, sahingga menstimulasi produksi globulin pengusung hormon seks lan ngalonake aktvitas enzim ing lintasa sintesis estrogen.
Nalika ngalami katabolisme, estrogen bakal mbentuk pira-pira senyawa intermediat kang disebut estrogen-katekol lewati 2 lintasan 2-hydroxylation karo enzim CYP1A1 lan 4-hydroxylation karo enzim CYP1B1,[4] kanggo dieliminasi kanti pira-pira proses kayata metilasi kanti enzim catechol-o-methyltransferase, hidroksilasi, oksidasi, detoksifikasi, sulfinasi kanti enzim sulfotransferase, lan glusuronidasi kanti enzim UGT. ing umumne senyawa estrogen-katekol duweni wektu paruh kang cendek amerga langsung termetilasi dadi 2-methoxyestradiol lan 4-methoxyestradiol. Senyawa estrogen-katekol isa duwen sifat tumorigenik utawa anti-tumorigenik, misale 4-hydroxyestradiol duweni sifat hormonal kanti ngaktivasi pencerap estrogen, lan nginduksi adenokarsinoma ing endometrium. Wondene 2-methyoxyestradiol duweni aktivitas antitumorigenik kanti ngalonake proliferasi lan angiogenesis ing sel tumor.
Cathetan sikil
- ↑ Fang H, Tong W, Shi L, Blair R, Perkins R, Branham W, Hass B, Xie Q, Dial S, Moland C, Sheehan D (2001). "Structure-activity relationships for a large diverse set of natural, synthetic, and environmental estrogens". Chem Res Toxicol. 14 (3): 280–94. PMID 11258977.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ↑ Masalah transklusi: {{En}} mung bisa kaanggo ing mandhala aran Barkas. Anggonen {{lang-en}} utawa {{en icon}} baé."Mechanisms of hormone carcinogenesis: evolution of views, role of mitochondria". Division of Pulmonary and Critical Care, Department of Medicine, University of Virginia School of Medicine; Chen JQ, Brown TR, Yager JD.(Kaunduh 30/1/13)
- ↑ Masalah transklusi: {{En}} mung bisa kaanggo ing mandhala aran Barkas. Anggonen {{lang-en}} utawa {{en icon}} baé."UGT1A1 Genetic Polymorphisms, Endogenous Estrogen Exposure, Soy Food Intake, and Endometrial Cancer Risk". Vanderbilt Epidemiology Center, Department of Medicine and Vanderbilt-Ingram Cancer Center, Nashville, Tennessee and Department of Epidemiology, Shanghai Cancer Institute, Cancer Institute of Shanghai Jiao Tong University; Sandra L. Deming, Wei Zheng, Wang-Hong Xu, Qiuyin Cai, Zhixian Ruan, Yong-Bing Xiang dan Xiao-Ou Shu.(Kaunduh 30/1/13)
- ↑ Masalah transklusi: {{En}} mung bisa kaanggo ing mandhala aran Barkas. Anggonen {{lang-en}} utawa {{en icon}} baé."Ovarian Cancer Risk and Polymorphisms Involved in Estrogen Catabolism". Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center; Department of Epidemiology, School of Public Health and Community Medicine; and Department of Otolaryngology-Head and Neck Surgery, School of Medicine, University of Washington; Sarah K. Holt, Mary Anne Rossing, Kathleen E. Malone, Stephen M. Schwartz, Noel S. Weiss and Chu Chen.(Kaunduh 30/1/13)