Diesel Exhaust Exposure Enhances the Persistence of Endometriosis Model in Rats

Masakazu Umezawa, Chika Sakata, Masako Tabata, Naomi Tanaka, Sayaka Kudo, Ken Takeda, Tomomi Ihara, Masao Sugamata
In: Journal of Health Science · 2008 · vol. 54(4) , pp. 503–507 · doi:10.1248/jhs.54.503 · W2169390361
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Diesel exhaust exposure during development increased the size of endometriotic lesions and elevated serum MCP-1 levels in a rat model of endometriosis.

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Abstract

Diesel exhaust (DE) is known to be one of the main causes of air pollution. Several studies have suggested that DE causes lung cancer, cardiovascular disease, abnormal reproductive function, and central nervous system damage as well as type I allergy in the airway. Type I allergy also plays a role in pathogenesis of endometriosis. In the present study, we examined the effect of exposure to DE on a rat model of endometriosis. Endometriosis was induced by autotransplantation of endometrium to the peritoneum in female Sprague-Dawley rats exposed to DE during prenatal and postnatal periods. Endometriotic lesions, normal peritoneum, and blood samples were obtained on days 4, 7, and 14 after autotransplantation. The extent of stromal proliferative lesions in the endometriosis model was greater in the rats of the DE exposure group than in those of the control group on day 14. Serum monocyte chemoattractant protein (MCP)-1 level was significantly higher in rats with endometriosis in the DE exposure group than in those in the control group on day 14. Results of this study suggest that DE exposure enhances the histologic and molecular pathology of endometriosis in rats.
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RAPID COMMUNICATIONS Diesel Exhaust Exposure Enhances the Persistence of Endometriosis Model in Rats 2008 Volume 54 Issue 4 Pages 503-507 Details Abstract Diesel exhaust (DE) is known to be one of the main causes of air pollution. Several studies have suggested that DE causes lung cancer, cardiovascular disease, abnormal reproductive function, and central nervous system damage as well as type I allergy in the airway. Type I allergy also plays a role in pathogenesis of endometriosis. In the present study, we examined the effect of exposure to DE on a rat model of endometriosis. Endometriosis was induced by autotransplantation of endometrium to the peritoneum in female Sprague-Dawley rats exposed to DE during prenatal and postnatal periods. Endometriotic lesions, normal peritoneum, and blood samples were obtained on days 4, 7, and 14 after autotransplantation. The extent of stromal proliferative lesions in the endometriosis model was greater in the rats of the DE exposure group than in those of the control group on day 14. Serum monocyte chemoattractant protein (MCP)-1 level was significantly higher in rats with endometriosis in the DE exposure group than in those in the control group on day 14. Results of this study suggest that DE exposure enhances the histologic and molecular pathology of endometriosis in rats. © 2008 by The Pharmaceutical Society of Japan Favorites & Alerts Recently viewed articles

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endometriosis

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