Action of the dioxin-like compound hexachlorobenzene in an experimental model of endometriosis in rats

MARCELA SUSANA SÁNCHEZ; FLORENCIA CHIAPPINI; MARIELA BILOTAS; CAROLINA PONTILLO; ELSA ZOTTA; CLAUDIA COCCA; GABRIELA MERESMAN; ANDREA SILVANA RANDI

Edimburgo

Congreso; 50th Congress of the European Societies of Toxicology, EUROTOX 2014; 2014

Sociedad Europea de Toxicología

Action of the dioxin-like compound hexachlorobenzene in an experimental model of endometriosis in rats. Sánchez MS1., Chiappini F1., Bilotas M2., Pontillo C1., Zotta E3., Cocca C4., Meresman G2., Randi A1. (1)Laboratorio de Efectos Biológicos de Contaminantes Ambientales, Depto de Bioquímica Humana, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina. (2) Laboratorio de Inmunología de la Reproducción, Instituto de Biología y Medicina Experimental, IBYME-CONICET, Buenos Aires, Argentina; (3) Laboratorio de Fisiopatogenia, Sección Patología, Depto de Ciencias Fisiológicas, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina; (4) Laboratorio de Radiosisótopos, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, Buenos Aires, Argentina; (5) Laboratorio de Fisiopatología Endometrial, Instituto de Biología y Medicina Experimental, IBYME-CONICET, Buenos Aires, Argentina. Hexachlorobenzene (HCB) is a dioxin-like environmental pollutant associated with a broad spectrum of toxic effects, including endocrine disruption and immunological disorders. Endometriosis is a gynecologic disease characterized by growth of endometrial tissue in ectopic sites, causing infertility in women of reproductive age. It has been proposed that endocrine-disrupting compounds could play a role in the onset or the growth of endometriosis. The severity of endometrial lesions is associated with expression of metalloproteases (MMPs). Inhibition of Cyclooxygenase-2 (COX-2) decreases invasion of ectopic lesions by suppressing MMP2-MMP9 activities. Besides, the development of the disease depends on the recruitment of new blood vessels. Our aim was to evaluate the effect of HCB on an experimentally induced endometriosis rat model. Fragments of endometrium were autotransplanted to the gut mesothelium of Sprague Dawley rats. Fifteen days post-surgery, rats were exposed to HCB (0, 1 and 100 mg/kg body weight) during 30 days. We analyzed endometriotic lesions (L) and eutopic endometrium (E), by evaluating vascular density by von Willebrand (VW+) immunohistochemistry; and MMPs and COX-2 expression by Western Blotting. We observed that HCB increases: a)endometriotic lesion volume (HCB100:107%,p