PMID- 16225763
OWN - NLM
STAT- MEDLINE
DCOM- 20070509
LR  - 20231213
IS  - 1671-4083 (Print)
IS  - 1671-4083 (Linking)
VI  - 26
IP  - 11
DP  - 2005 Nov
TI  - Alterations of placental cytochrome P450 1A1 and P-glycoprotein in 
      tobacco-induced intrauterine growth retardation in rats.
PG  - 1387-94
AB  - AIM: To investigate the alterations of placental P-glycoprotein (P-gp) and 
      cytochrome P450 1A1 (CYP1A1) at different gestational days (GD), and to explore 
      the possible significance of placental P-gp and CYP1A1 in tobacco smoke-induced 
      intrauterine growth retardation (IUGR) in rats. METHODS: An IUGR model was 
      produced by passive tobacco smoking from GD7 to parturition (GD21) and predicted 
      using fetal development parameters. Placental structure and function were 
      monitored by observing pathological alteration and antioxidative function, 
      including the content of malondialdehyde and the activities of superoxide 
      dismutase and catalase (CAT). The expressions of CYP1A1 and P-gp (mdr 1a and mdr 
      1b) were detected using a reverse transcription polymerase chain reaction and 
      immunohistochemistry. RESULTS: Placental pathological changes occurred and the 
      malondialdehyde content increased, whereas the activities of superoxide dismutase 
      and CAT lowered, when compared to their controls. In the rat placenta of the 
      tobacco group, the level of CYP1A1 mRNA increased significantly; the level of 
      mdr1a mRNA increased significantly at GD21 but not at GD14, whereas the level of 
      mdr1b mRNA in different term remained stable; the expression of P-gp increased 
      significantly only in full-term placenta. CONCLUSION: The expression of placental 
      CYP1A1 and P-gp increased in tobacco-induced IUGR. Overexpression of placental 
      CYP1A1 can attribute to the metabolism of tobacco and the generation of reactive 
      metabolites, which can trigger IUGR. As a compulsory mechanism, upregulation of 
      P-gp might decrease tobacco exposure to a developing fetus with IUGR.
FAU - Yan, You-e
AU  - Yan YE
AD  - Department of Pharmacology, Medical College of Wuhan University, Wuhan 430071, 
      China.
FAU - Wang, Hui
AU  - Wang H
FAU - Feng, Ying-hong
AU  - Feng YH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Acta Pharmacol Sin
JT  - Acta pharmacologica Sinica
JID - 100956087
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B)
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (ATP-Binding Cassette Transporters)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tobacco Smoke Pollution)
RN  - 9EI49ZU76O (multidrug resistance protein 3)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B/biosynthesis/genetics
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/*biosynthesis/genetics
MH  - ATP-Binding Cassette Transporters/biosynthesis/genetics
MH  - Animals
MH  - Cytochrome P-450 CYP1A1/*biosynthesis/genetics
MH  - Female
MH  - Fetal Growth Retardation/etiology/*metabolism/pathology
MH  - Placenta/metabolism/*pathology
MH  - Pregnancy
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Tobacco Smoke Pollution/*adverse effects
MH  - ATP-Binding Cassette Sub-Family B Member 4
EDAT- 2005/10/18 09:00
MHDA- 2007/05/10 09:00
CRDT- 2005/10/18 09:00
PHST- 2005/10/18 09:00 [pubmed]
PHST- 2007/05/10 09:00 [medline]
PHST- 2005/10/18 09:00 [entrez]
AID - 10.1111/j.1745-7254.2005.00209.x [doi]
PST - ppublish
SO  - Acta Pharmacol Sin. 2005 Nov;26(11):1387-94. doi: 
      10.1111/j.1745-7254.2005.00209.x.