Inhibition of Human Polymorphonuclear Cell Oxidative Burst by 17-β-estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin
Article first published online: 5 NOV 2003
American Journal of Reproductive Immunology
Volume 50, Issue 6, pages 463–472, December 2003
How to Cite
Abrahams, V. M., Collins, J. E., Wira, C. R., Fanger, M. W. and Yeaman, G. R. (2003), Inhibition of Human Polymorphonuclear Cell Oxidative Burst by 17-β-estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin. American Journal of Reproductive Immunology, 50: 463–472. doi: 10.1046/j.8755-8920.2003.00111.x
- Issue published online: 5 NOV 2003
- Article first published online: 5 NOV 2003
- Submitted March 18, 2003; revised May 28, 2003; accepted May 30, 2003.
- Aryl hydrocarbon receptor;
- estrogen receptor;
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.