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Inhibition of Human Polymorphonuclear Cell Oxidative Burst by 17‐β‐estradiol and 2,3,7,8‐tetrachlorodibenzo‐ p ‐dioxin
Author(s) -
Abrahams Vikki M.,
Collins Jane E.,
Wira Charles R.,
Fanger Michael W.,
Yeaman Grant R.
Publication year - 2003
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1046/j.8755-8920.2003.00111.x
Subject(s) - superoxide , respiratory burst , endocrinology , medicine , aryl hydrocarbon receptor , lucigenin , chemistry , phorbol , estrogen , estrogen receptor , neutrophile , receptor , granulocyte , endocrine disruptor , endocrine system , in vitro , hormone , biology , protein kinase c , biochemistry , signal transduction , enzyme , cancer , breast cancer , gene , transcription factor
Problem: Polymorphonuclear cell (PMN) function may be directly influenced by 17‐ β ‐estradiol and the endocrine disruptor, 2,3,7,8‐tetrachloro‐dibenzo‐ p ‐dioxin (TCDD). This may have significant consequences on PMN function within the female reproductive tract. This study evaluated the effects of 17‐ β ‐estradiol and TCDD on PMN oxidative burst. Method of study: Peripheral blood PMN were isolated from normal male donors. Following treatment with 17‐ β ‐estradiol, TCDD or both, PMN were stimulated with phorbol 12‐myristate 13‐acetate. Superoxide production was measured by lucigenin‐enhanced chemiluminescence. Results: Following 24‐hr culture with either 17‐ β ‐estradiol or TCDD, PMN superoxide production was significantly reduced, however, no such inhibition was observed when PMN were cultured with both estradiol and TCDD. Using antagonists, the estradiol and TCDD effects on PMN superoxide production was shown to be estrogen and aryl hydrocarbon receptor mediated. Conclusions: Estradiol and TCDD influence PMN oxidative burst through receptor mediated events. Such altered PMN function may have profound effects upon the normal endometrial cycle.