期刊
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 233, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.113347
关键词
Benzophenone-3; Spontaneous fetal loss; Metabolomics
资金
- National Key Research and Devel-opment Program of China [2018YFC1004201]
- National Natural Science Foundation of China [81872650, 81573182]
- Key Natural Science Foundation of the Jiangsu Higher Education Institutions of China [18KJA320003]
- Key Research & Development Plan of Jiangsu Province [BE2017628]
- Nanjing Medical Science and Technique Development Foundation [QRX17162]
- Nanjing Medical Science and Technology Development Fund [ZKX19044]
- Southeast University & Nanjing Medical University Collaborative Research Project [2242018K3DN25, 2018DN002]
- Innovation Fund Project of the State Key Laboratory of Reproductive Medicine [SKLRM-GC2020B1, SKLRM-GC201901]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
Benzophenone-3 (BP-3) is widely used in cosmetics and women are exposed to high levels of BP-3. This study investigated the effects of BP-3 on fetal and uterine metabolism in mice, and found that it can induce placental thrombosis and fetal loss through disturbances in metabolism.
Benzophenone-3 (BP-3) is widely used in a variety of cosmetics and is prevalent in drinking water or food, and women were under notable high exposure burden of BP-3. Reports show the associations between prenatal exposure to BP-3 and the risk of fetal loss, but its underlying mechanism remains largely unknown. Pregnant ICR mice were gavaged with BP-3 from gestational day (GD) 0 to GD 6 at doses of 0.1, 10 and 1000 mg/kg/day. The samples were collected on GD 12. Ultra-performance liquid chromatography coupled with mass spectrometry based metabolomics was used to detect metabolome changes in fetal mice, the uterus and the placenta to identify the underlying mechanism. The results showed that the body weight and relative organ weights of the liver, brain and uterus of pregnant mice were not significantly changed between the control group and the treatment group. BP-3 increased fetal loss, and induced placental thrombosis and tissue necrosis with enhancement of platelet aggregation. Metabolomic analysis revealed that fructose and mannose metabolism, the TCA cycle, arginine and proline metabolism in the fetus, arginine and proline metabolism and biotin metabolism in the uterus, and arginine biosynthesis and pyrimidine metabolism in the placenta were the key changed pathways involved in the above changes. Our study indicates that exposure to BP-3 can induce placental thrombosis and fetal loss via the disruption of maternal and fetal metabolism in mice, providing novel insights into the influence of BP-3 toxicity on the female reproductive system.
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