PMID- 11307634
OWN - NLM
STAT- MEDLINE
DCOM- 20010816
LR  - 20191104
IS  - 0148-0545 (Print)
IS  - 0148-0545 (Linking)
VI  - 24
IP  - 1
DP  - 2001 Feb
TI  - Placebo-controlled, blinded comparison of antenatal betamethasone on mouse liver 
      development.
PG  - 49-61
AB  - The objective of this investigation was to evaluate, in a placebo-controlled 
      manner, the developing mouse liver after antenatal exposure either to a single 
      dose or to a multidose of betamethasone. Ninety gravid CD-1 mice were randomly 
      divided into three groups (n = 30/group) to receive either saline (0.25 mL s.c.) 
      or betamethasone (0.10 mg s.c.) as a single dose on gestational day (GD) 14 of a 
      19-day gestation or as a 0.10 mg dose given twice daily on GD 14 and on GD 15 (4 
      doses). GD 0 is defined by the presence of a copulatory plug. These exposures of 
      betamethasone cause fetal mouse lung maturation as would be observed in premature 
      humans at 24-34 weeks of gestation. The livers were removed either from the 
      fetuses on GD 16.5 or from the offspring on postnatal day 1, 3, 5, and 120. 
      Special stains were used to evaluate hepatocyte architecture, glycoprotein and 
      glycogen content, extramedullary hematopoiesis and iron storage. Hepatocyte 
      intranuclear DNA content, cell size, and cell shape were measured by image 
      analysis (CAS 200). At GD 16.5, betamethasone produced a significant decrease in 
      the liver/body weight ratio that, when compared with the placebo group, was 
      greater with the multidose (p < 0.01) than with the single dose (p < 0.05). 16.5 
      GD single dose hepatocytes were smaller in size as compared to placebo without 
      impact on intranuclear DNA (p < 0.01). Single dose PND 1 hepatocytes demonstrated 
      an increase in intranuclear DNA as compared to placebo but without change in cell 
      size (p < 0.001). The prenatal reduced liver weight recovered in the newborn 
      period. No difference in microscopic architecture of the hepatocytes or 
      histologic differences between either of the three treatment groups was found in 
      glycogen deposition, extramedullary hematopoiesis or iron metabolism at GD 16.5 
      and postnatally. It was concluded antenatal betamethasone can cause a decrease in 
      the liver/body weight ratio in the fetal mouse that recovers eventually without 
      any functional impact as assessed histologically.
FAU - Sienko, A E
AU  - Sienko AE
AD  - University of Oklahoma Health Sciences Center, Department of Pathology, BMSB Room 
      451, 940 Stanton Young Blvd., Oklahoma City, OK 73104, USA. 
      anna-sienko@uokhsc.edu
FAU - Stewart, J D
AU  - Stewart JD
FAU - Gonzalez, C L
AU  - Gonzalez CL
FAU - Christensen, H D
AU  - Christensen HD
FAU - Lerner, M
AU  - Lerner M
FAU - Rayburn, W F
AU  - Rayburn WF
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Drug Chem Toxicol
JT  - Drug and chemical toxicology
JID - 7801723
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Placebos)
RN  - 451W47IQ8X (Sodium Chloride)
RN  - 9007-49-2 (DNA)
RN  - 9842X06Q6M (Betamethasone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/administration & dosage/*pharmacology/toxicity
MH  - Betamethasone/administration & dosage/*pharmacology/toxicity
MH  - Body Weight/drug effects
MH  - DNA/drug effects
MH  - Embryonic and Fetal Development/*drug effects
MH  - Female
MH  - Hepatocytes/cytology/drug effects
MH  - Litter Size/drug effects
MH  - Liver/cytology/*drug effects/embryology/growth & development
MH  - Lung/drug effects/embryology
MH  - Male
MH  - Mice
MH  - Organ Size/drug effects
MH  - Placebos
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects
MH  - Random Allocation
MH  - Sodium Chloride/pharmacology
EDAT- 2001/04/20 10:00
MHDA- 2001/08/17 10:01
CRDT- 2001/04/20 10:00
PHST- 2001/04/20 10:00 [pubmed]
PHST- 2001/08/17 10:01 [medline]
PHST- 2001/04/20 10:00 [entrez]
AID - 10.1081/dct-100103085 [doi]
PST - ppublish
SO  - Drug Chem Toxicol. 2001 Feb;24(1):49-61. doi: 10.1081/dct-100103085.