Dioxin may promote inflammation-related development of endometriosis

被引：47

作者：

Bruner-Tran, Kaylon L. ^{[1
]}

Yeaman, Grant R. ^{[1
]}

Crispens, Marta A. ^{[1
]}

Igarashi, Toshio M. ^{[1
]}

Osteen, Kevin G. ^{[1
]}

机构：

[1] Vanderbilt Univ, Sch Med, Womens Reprod Hlth Res Ctr, Dept Obstet & Gynecol, Nashville, TN 37232 USA

来源：

FERTILITY AND STERILITY | 2008年 / 89卷

关键词：

endometriosis; dioxin; progesterone; inflammation; leukocytes;

D O I：

10.1016/j.fertnstert.2008.02.102

中图分类号：

R71 [妇产科学];

学科分类号：

100211 ;

摘要：

Laboratory and population-based studies suggest that exposure to environmental toxicants may be one of several triggers for the development of endometriosis. We discuss evidence that modulation of the endometrial endocrine-immune interface could mechanistically link toxicant exposure to the development of this disease.

引用

页码：1287 / 1298

页数：12

共 134 条

[1] Inhibition of human polymorphonuclear cell oxidative burst by 17-β-estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin [J].

Abrahams, VM ;

Collins, JE ;

Wira, CR ;

Fanger, MW ;

Yeaman, GR .

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, 2003, 50 (06) :463-472

[2]

ABRAHAMS VM, 2000, ORGANOHALOGEN COMPOU, V49, P377

[3] Vascular endothelial growth factor VEGF189 induces human neutrophil chemotaxis in extravascular tissue via an autocrine amplification mechanism [J].

Ancelin, M ;

Chollet-Martin, S ;

Hervé, MA ;

Legrand, C ;

El Benna, J ;

Perrot-Applanat, M .

LABORATORY INVESTIGATION, 2004, 84 (04) :502-512

[4] A dynamic shift of VEGF isoforms with a transient and selective progesterone-induced expression of VEGF189 regulates angiogenesis and vascular permeability in human uterus [J].

Ancelin, M ;

Buteau-Lozano, H ;

Meduri, G ;

Osborne-Pellegrin, M ;

Sordello, S ;

Plouët, J ;

Perrot-Applanat, M .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (09) :6023-6028

[5] Progesterone receptor isoform A but not B is expressed in endometriosis [J].

Attia, GR ;

Zeitoun, K ;

Edwards, D ;

Johns, A ;

Carr, BR ;

Bulun, SE .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2000, 85 (08) :2897-2902

[6] Critical role for lysines 21 and 22 in signal-induced, ubiquitin-mediated proteolysis of I kappa B-alpha [J].

Baldi, L ;

Brown, K ;

Franzoso, G ;

Siebenlist, U .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (01) :376-379

[7] Non-carcinogenic effects of TCDD in animals [J].

Birnbaum, LS ;

Tuomisto, J .

FOOD ADDITIVES AND CONTAMINANTS PART A-CHEMISTRY ANALYSIS CONTROL EXPOSURE & RISK ASSESSMENT, 2000, 17 (04) :275-288

[8] THE MECHANISM OF DIOXIN TOXICITY - RELATIONSHIP TO RISK ASSESSMENT [J].

BIRNBAUM, LS .

ENVIRONMENTAL HEALTH PERSPECTIVES, 1994, 102 :157-167

[9] Effect of TCDD exposure on CYP1A1 and CYP1B1 expression in explant cultures of human endometrium [J].

Bofinger, DP ;

Feng, L ;

Chi, LH ;

Love, J ;

Stephen, FD ;

Sutter, TR ;

Osteen, KG ;

Costich, TG ;

Batt, RE ;

Koury, ST ;

Olson, JR .

TOXICOLOGICAL SCIENCES, 2001, 62 (02) :299-314

[10]

BOYD J, 1995, END 2000 MAY 15 17 B

← 1 2 3 4 5 6 7 8 9 10 →