PMID- 1948765
OWN - NLM
STAT- MEDLINE
DCOM- 19911223
LR  - 20131121
IS  - 0040-3709 (Print)
IS  - 0040-3709 (Linking)
VI  - 44
IP  - 3
DP  - 1991 Sep
TI  - Pathogenesis of ethanol-induced hydronephrosis and hydroureter as demonstrated 
      following in vivo exposure of mouse embryos.
PG  - 299-312
AB  - Urinary tract abnormalities have been noted to occur in 10-27% of individuals 
      diagnosed as having Fetal Alcohol Syndrome. Among a wide range of functional and 
      structural abnormalities, renal agenesis/hypoplasia, hydronephrosis, and 
      ureteropelvic obstruction feature most prominently. This study was designed to 
      examine the pathogenesis of ethanol-induced urinary tract abnormalities in a 
      mouse model. C57Bl/6J mice were acutely exposed to two doses of ethanol (2.9 g/kg 
      IP) administered 4 hours apart beginning on gestational day (GD) 9, hour 4. This 
      resulted in an incidence of 40.7% urinary tract anomalies among GD18 fetuses. 
      With the exception of duplicate ureter, urinary tract abnormalities consisted 
      exclusively of hydroureter/hydronephrosis. Examination of GD13-17 fetuses 
      revealed that the first grossly detectable differences in the urinary tracts of 
      control vs. affected specimens occurred on GD16 and initially only involved 
      ureteral changes. Hydronephrosis was first detected on GD17. A contributing 
      factor to the development of hydronephrosis appears to be the abnormal location 
      of the ureterovesicle junction which commonly involves duplicate ureteral lumens 
      with resultant functional obstruction to urine flow at the distal end of the 
      ureter. Study of the early pathogenetic changes which appear to result in the 
      urinary tract malformations observed involved utilization of scanning electron 
      microscopy, vital dye (Nile blue sulphate) staining of whole embryos, and 
      analysis of histological sections. These studies revealed that 12 hours following 
      initial maternal ethanol exposure, embryos have excessive amounts of cell death 
      localized in the region of the developing mesonephric duct just proximal to the 
      cloaca. Also affected were premigratory neural crest cells located just proximal 
      to the posterior neuropore. We conclude that excessive amounts of ethanol-induced 
      cell death in these selectively vulnerable populations could account for the 
      subsequently observed urinary tract malformations.
FAU - Gage, J C
AU  - Gage JC
AD  - Department of Cell Biology and Anatomy, University of North Carolina, Chapel Hill 
      27599-7090.
FAU - Sulik, K K
AU  - Sulik KK
LA  - eng
GR  - AA08204/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Teratology
JT  - Teratology
JID - 0153257
SB  - IM
MH  - Abnormalities, Drug-Induced/*etiology
MH  - Animals
MH  - Embryo, Mammalian/*drug effects
MH  - Female
MH  - Fetal Alcohol Spectrum Disorders/*complications
MH  - Gestational Age
MH  - Hydronephrosis/*etiology
MH  - Maternal-Fetal Exchange/*drug effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Phenotype
MH  - Pregnancy
MH  - Ureteral Diseases/*etiology
MH  - Urogenital Abnormalities
EDAT- 1991/09/01 00:00
MHDA- 1991/09/01 00:01
CRDT- 1991/09/01 00:00
PHST- 1991/09/01 00:00 [pubmed]
PHST- 1991/09/01 00:01 [medline]
PHST- 1991/09/01 00:00 [entrez]
AID - 10.1002/tera.1420440307 [doi]
PST - ppublish
SO  - Teratology. 1991 Sep;44(3):299-312. doi: 10.1002/tera.1420440307.