PMID- 16263228
OWN - NLM
STAT- MEDLINE
DCOM- 20060502
LR  - 20131121
IS  - 0378-4274 (Print)
IS  - 0378-4274 (Linking)
VI  - 163
IP  - 1
DP  - 2006 May 5
TI  - Tumor necrosis factor alpha partially contributes to lipopolysaccharide-induced 
      intra-uterine fetal growth restriction and skeletal development retardation in 
      mice.
PG  - 20-9
AB  - Maternal infection is a cause of adverse developmental outcomes. 
      Lipopolysaccharide (LPS)-induced embryonic resorption, intra-uterine fetal death 
      (IUFD) and preterm labor have been well characterized. In the present study, we 
      investigated the effects of maternal LPS exposure on intra-uterine fetal growth 
      and skeletal development. All pregnant mice except controls received an 
      intraperitoneal injection of LPS (75 microg/kg) on gestational days (GD) 15-17. 
      The number of live fetuses, dead fetuses and resorption sites was counted on GD 
      18. Live fetuses in each litter were weighed. Crown-rump and tail lengths were 
      examined and skeletal development was evaluated. As expected, perinatal LPS 
      exposure resulted in 63.2% fetal death. LPS significantly lowered fetal weight, 
      reduced crown-rump and tail lengths, and retarded skeletal ossification in caudal 
      vertebrae, anterior and posterior phalanges, and supraoccipital bone. Additional 
      experiment showed that a single dose of LPS (75 microg/kg, i.p.) on GD 15 
      increased the expression of TNF-alpha mRNA in maternal liver and placenta and 
      TNF-alpha concentration in maternal serum and amniotic fluid. Furthermore, 
      pentoxifylline, an inhibitor of TNF-alpha synthesis, significantly inhibited 
      TNF-alpha production, reduced fetal mortality, and reversed LPS-induced fetal 
      intra-uterine growth restriction and skeletal development retardation. Taken 
      together, these results suggest that TNF-alpha is, at least in part, involved in 
      LPS-induced intra-uterine fetal death, intra-uterine growth restriction and 
      skeletal development retardation.
FAU - Xu, De-Xiang
AU  - Xu DX
AD  - Department of Toxicology, Anhui Medical University, Hefei 230032, PR China. 
      xudex@mail.hf.ah.cn
FAU - Chen, Yuan-Hua
AU  - Chen YH
FAU - Wang, Hua
AU  - Wang H
FAU - Zhao, Lei
AU  - Zhao L
FAU - Wang, Jian-Ping
AU  - Wang JP
FAU - Wei, Wei
AU  - Wei W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20051102
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Amniotic Fluid/metabolism
MH  - Animals
MH  - Female
MH  - Fetal Development/*drug effects
MH  - Fetal Growth Retardation
MH  - Fetal Weight/drug effects
MH  - Gene Expression Regulation/drug effects
MH  - Glutathione/metabolism
MH  - Lipid Peroxidation/drug effects
MH  - Lipopolysaccharides/*toxicity
MH  - Male
MH  - *Maternal Exposure
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Osteogenesis/*drug effects
MH  - Pregnancy
MH  - RNA, Messenger/biosynthesis
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/genetics
EDAT- 2005/11/03 09:00
MHDA- 2006/05/04 09:00
CRDT- 2005/11/03 09:00
PHST- 2005/07/25 00:00 [received]
PHST- 2005/09/10 00:00 [revised]
PHST- 2005/09/12 00:00 [accepted]
PHST- 2005/11/03 09:00 [pubmed]
PHST- 2006/05/04 09:00 [medline]
PHST- 2005/11/03 09:00 [entrez]
AID - S0378-4274(05)00276-6 [pii]
AID - 10.1016/j.toxlet.2005.09.009 [doi]
PST - ppublish
SO  - Toxicol Lett. 2006 May 5;163(1):20-9. doi: 10.1016/j.toxlet.2005.09.009. Epub 
      2005 Nov 2.