Endocrine disruptor, dioxin (TCDD)-induced mitochondrial dysfunction and apoptosis in human trophoblast-like JAR cells-Reference-Cited by-同舟云学术

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Endocrine disruptor, dioxin (TCDD)-induced mitochondrial dysfunction and apoptosis in human trophoblast-like JAR cells

Published:2010-01-18 Issue:5 Volume:16 Page:361-372
ISSN:1360-9947
Container-title:Molecular Human Reproduction
language:en
Short-container-title:Molecular Human Reproduction

Author:

Chen S. C.,Liao T. L.,Wei Y. H.,Tzeng C. R.,Kao S. H.

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Developmental Biology,Obstetrics and Gynecology,Genetics,Molecular Biology,Embryology,Reproductive Medicine

Link

http://academic.oup.com/molehr/article-pdf/16/5/361/6279104/gaq004.pdf

Reference54 articles.

1. Oxidative stress, sperm survival and fertility control

2. A constitutively active dioxin/aryl hydrocarbon receptor induces stomach tumors

3. Comparison of accumulation and altered steroid secretion by placental tissue treated with TCDD and natural mixture of PCDDs-PCDFs

4. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) accelerates differentiation of murine preimplantation embryos in vitro

5. Maternal smoking is associated with mitochondrial DNA depletion and respiratory chain complex III deficiency in placenta

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