Pathological study for the effects of in utero and postnatal exposure to diesel exhaust on a rat endometriosis model

Masakazu Umezawa, Chika Sakata, Naomi Tanaka, Masako Tabata, Ken Takeda, Tomomi Ihara, Masao Sugamata
The Journal of toxicological sciences · 2011 · vol. 36(4) , pp. 493–498 · doi:10.2131/jts.36.493 · PMID:21804314 · W2050560144
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Prenatal and postnatal diesel exhaust exposure in a rat endometriosis model increased mast cell activation and prolonged collagen fiber persistence around endometriotic lesions.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This pathological study investigated how prenatal and postnatal exposure to diesel exhaust affects an induced rat endometriosis model. Pregnant Sprague-Dawley rats were exposed to diesel exhaust or clean air from gestational day 2, and neonatal rats were persistently exposed similarly; endometriosis was then created by autotransplantation of endometrium onto the peritoneum of female offspring, with lesions examined 7 and 14 days after transplantation. The authors found that compared with controls, diesel exhaust exposure led to infiltration of activated mast cells in deeper peritoneal tissue at 14 days, and that at 14 days the remaining lesions contained fibroblasts and activated mast cells surrounded by collagen fibers, indicating enhanced mast cell activation and prolonged persistence of collagen fibers. The paper notes only the observed histopathological effects at these early post-transplant time points as its limitation. This paper is centrally about endometriosis — it tests whether in utero and postnatal diesel exhaust exposure alters mast cell activation and lesion persistence in a rat endometriosis model.

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Abstract

Previous studies have shown that prenatal and postnatal exposure to diesel exhaust (DE), which is known to be one of the main constituents of air pollution, enhances the persistence of endometriosis in a rat model. The aim of this study is to investigate the pathological changes induced by DE exposure in a rat model of endometriosis. Pregnant Sprague-Dawley rats were exposed to DE or clean air beginning on gestational day 2 and neonatal rats were persistently exposed to DE or clean air. Endometriosis was induced by autotransplantation of endometrium onto the peritoneum of eight-week-old female offspring. Endometriotic lesions were examined at 7 and 14 days post-transplantation. As a result, infiltration of activated mast cells remained in deeper area of peritoneal tissue around the endometriosis model compared to the control group at 14 days post-autotransplantation. In the DE exposure group, 14 days post-transplant, the remaining lesions contained fibroblasts and activated mast cells, which were surrounded by collagen fibers. The data showed that prenatal and postnatal DE exposure enhances the activation of mast cells and prolongs the persistence of collagen fibers in the induced rat model of endometriosis.
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Letter Pathological study for the effects of in utero and postnatal exposure to diesel exhaust on a rat endometriosis model 2011 Volume 36 Issue 4 Pages 493-498 Details Abstract Previous studies have shown that prenatal and postnatal exposure to diesel exhaust (DE), which is known to be one of the main constituents of air pollution, enhances the persistence of endometriosis in a rat model. The aim of this study is to investigate the pathological changes induced by DE exposure in a rat model of endometriosis. Pregnant Sprague-Dawley rats were exposed to DE or clean air beginning on gestational day 2 and neonatal rats were persistently exposed to DE or clean air. Endometriosis was induced by autotransplantation of endometrium onto the peritoneum of eight-week-old female offspring. Endometriotic lesions were examined at 7 and 14 days post-transplantation. As a result, infiltration of activated mast cells remained in deeper area of peritoneal tissue around the endometriosis model compared to the control group at 14 days post-autotransplantation. In the DE exposure group, 14 days post-transplant, the remaining lesions contained fibroblasts and activated mast cells, which were surrounded by collagen fibers. The data showed that prenatal and postnatal DE exposure enhances the activation of mast cells and prolongs the persistence of collagen fibers in the induced rat model of endometriosis. 2011 The Japanese Society of Toxicology Favorites & Alerts Recently viewed articles

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Air Pollutants Endometriosis Endometriosis Prenatal Exposure Delayed Effects Prenatal Exposure Delayed Effects Vehicle Emissions Air Pollutants Animals Animals, Newborn Disease Models, Animal Endometriosis Endometrium Endometrium Endometrium Endometrium Female Fibroblasts Fibroblasts Fibroblasts Gestational Age

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