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Updated: Jan 22, 2026

Analysis of Electrocardiograms and Behavior in Mice from Pregnancy to Lactation Period
Published on: April 5, 2024
Cardiotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure through lactation in mice
Nozomi Fujisawa1, Chiharu Tohyama1,2, Wataru Yoshioka1,3
1Laboratory of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo.
Exposure to dioxin (TCDD) during early development causes progressive heart hypertrophy and fibrosis in mice. Key genes like ANP, β-MHC, and ET-1 may mediate this dioxin-induced cardiotoxicity.
Area of Science:
- Environmental Toxicology
- Cardiovascular Research
- Developmental Biology
Background:
- Dioxins are persistent environmental pollutants.
- 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a highly toxic dioxin congener.
- TCDD exposure is linked to cardiac diseases and cardiotoxicity in animal models.
Purpose of the Study:
- To characterize TCDD-induced cardiotoxicity during the postnatal developmental period.
- To investigate the effects of TCDD on developing mouse hearts.
Main Methods:
- Mouse pups were exposed to TCDD (0, 20, or 80 μg/kg) via maternal administration.
- Histological and gene expression analyses were performed on postnatal days 7 and 21.
- Evaluated left ventricular remodeling, heart hypertrophy, fibrosis, and specific gene markers.
Main Results:
- TCDD exposure led to left ventricular remodeling by postnatal day 7.
- Progressive heart hypertrophy and fibrosis were observed by postnatal day 21 in the TCDD-80 group.
- Increased expression of atrial natriuretic peptide (ANP), β-myosin heavy chain (β-MHC), and endothelin-1 (ET-1) was noted.
Conclusions:
- TCDD directly induces cardiotoxicity in the postnatal period.
- The observed cardiac hypertrophy is progressive and associated with fibrosis.
- ANP, β-MHC, and ET-1 may play roles in mediating TCDD-induced cardiac hypertrophy and heart failure.
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