PMID- 22484357
OWN - NLM
STAT- MEDLINE
DCOM- 20120612
LR  - 20131121
IS  - 1879-3185 (Electronic)
IS  - 0300-483X (Linking)
VI  - 296
IP  - 1-3
DP  - 2012 Jun 14
TI  - High dose bisphenol A impairs hippocampal neurogenesis in female mice across 
      generations.
PG  - 73-82
LID - 10.1016/j.tox.2012.03.007 [doi]
AB  - Bisphenol A (BPA) is used as a monomer during the manufacture of polycarbonate 
      plastics and epoxy resins. However, BPA adversely affects reproductive organ 
      growth and development, and it has been proposed that the detrimental effects of 
      BPA could extend to future generations. The present study was conducted to 
      evaluate the transgenerational effects of BPA on hippocampal neurogenesis and 
      neurocognitive function. Pregnant female C57BL/6 mice (F0) were exposed to BPA 
      (0.1-10 mg/kg) from gestation day 6 to 17, and female offspring (F2) from F1 
      generation mice were prepared. It was found that exposure of F0 mice to BPA at 10 
      mg/kg decreased the number of newly generated cells in the hippocampi of F2 
      female mice. Passive avoidance testing revealed that high-doses BPA (1 mg/kg and 
      10 mg/kg) decreased cross-over latency time in F2 mice, suggesting a BPA-mediated 
      neurocognitive deficit in terms of memory retention. Furthermore, it was found 
      that levels of phospho-ERK, brain-derived neurotrophic factor (BDNF), and 
      phospho-CREB in hippocampi were significantly lower in F2 mice. Interestingly, 
      the effects of BPA on hippocampal neurogenesis were found to be correlated with 
      altered DNA methylation. In particular, high-dose BPA exposure increased DNA 
      methylation of the CREB regulated transcription coactivator 1 (Crtc1) generated 
      in F2 mice. These findings suggest that BPA exposure of pregnant mothers could 
      adversely affect hippocampal neurogenesis and cognitive function in future 
      generations by modulating the ERK and BDNF-CREB signaling cascades.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Jang, Young Jung
AU  - Jang YJ
AD  - Department of Pharmacy, College of Pharmacy and Research Institute for Drug 
      Development, Longevity Life Science and Technology Institutes, Pusan National 
      University, Geumjeong-gu, Busan 609-735, Republic of Korea.
FAU - Park, Hee Ra
AU  - Park HR
FAU - Kim, Tae Hyung
AU  - Kim TH
FAU - Yang, Wook-Jin
AU  - Yang WJ
FAU - Lee, Jong-Joo
AU  - Lee JJ
FAU - Choi, Seon Young
AU  - Choi SY
FAU - Oh, Shin Bi
AU  - Oh SB
FAU - Lee, Eunjin
AU  - Lee E
FAU - Park, Joo-Hong
AU  - Park JH
FAU - Kim, Hyoung-Pyo
AU  - Kim HP
FAU - Kim, Hyung Sik
AU  - Kim HS
FAU - Lee, Jaewon
AU  - Lee J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120403
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Benzhydryl Compounds)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Creb1 protein, mouse)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Endocrine Disruptors)
RN  - 0 (Estrogens, Non-Steroidal)
RN  - 0 (Phenols)
RN  - MLT3645I99 (bisphenol A)
SB  - IM
MH  - Animals
MH  - Benzhydryl Compounds
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cognition/drug effects
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Endocrine Disruptors/*toxicity
MH  - Estrogens, Non-Steroidal/*toxicity
MH  - Female
MH  - Hippocampus/cytology/*drug effects/physiology
MH  - Learning/drug effects
MH  - Maternal-Fetal Exchange
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurogenesis/*drug effects
MH  - Phenols/*toxicity
MH  - Pregnancy
EDAT- 2012/04/10 06:00
MHDA- 2012/06/13 06:00
CRDT- 2012/04/10 06:00
PHST- 2012/01/30 00:00 [received]
PHST- 2012/03/21 00:00 [revised]
PHST- 2012/03/23 00:00 [accepted]
PHST- 2012/04/10 06:00 [entrez]
PHST- 2012/04/10 06:00 [pubmed]
PHST- 2012/06/13 06:00 [medline]
AID - S0300-483X(12)00094-7 [pii]
AID - 10.1016/j.tox.2012.03.007 [doi]
PST - ppublish
SO  - Toxicology. 2012 Jun 14;296(1-3):73-82. doi: 10.1016/j.tox.2012.03.007. Epub 2012 
      Apr 3.