PMID- 9294722
OWN - NLM
STAT- MEDLINE
DCOM- 19971017
LR  - 20220317
IS  - 0091-6765 (Print)
IS  - 0091-6765 (Linking)
VI  - 105
IP  - 7
DP  - 1997 Jul
TI  - Promotion of endometriosis in mice by polychlorinated dibenzo-p-dioxins, 
      dibenzofurans, and biphenyls.
PG  - 750-5
AB  - Previous studies showed exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin 
      (2,3,7,8-TCDD) enhances the development of endometriotic lesions. In this study 
      we examined the effects of other polyhalogenated aromatic hydrocarbons on 
      endometriotic proliferation. B6C3F1 female mice were treated via oral gavage a 
      total of five times, with 3 weeks between each dosing, with 0, 1, 3, or 10 
      micrograms 2,3,7,8,-TCDD/kg body weight (bw); 3 or 30 mg 
      2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153)/kg bw; 100, 300, or 1000 micrograms 
      3,3',4,4',5-pentachlorobiphenyl (PCB 126)/kg bw; 10, 30, or 100 micrograms 
      2,3,4,7,8-pentachlorodibenzofuran (4-PeCDF)/kg bw; or 2 or 20 mg 1,3,6,8-TCDD/kg 
      at 10 ml/kg bw. Endometriosis was surgically induced during the week of the 
      second dosing. Three weeks following the final dose, the mice were euthanized and 
      endometriotic lesions, whole body, liver, ovaries, uterine horn, and thymus were 
      weighted, and lesion diameters were measured. Lesions, uterine horns, and ovaries 
      were fixed for histopathology and livers were processed for measurement of 
      ethoxyresorufin O-deethylase (EROD) activity. Both 2,3,7,8-TCDD (1 and 3 
      micrograms/kg bw) and 4-PeCDF (100 micrograms/kg bw) significantly enhanced the 
      growth of endometrial lesions. No statistically significant increase in 
      endometriotic lesion size was detected in animals treated with either PCB 126 or 
      with the highest dose of 2,3,7,8-TCDD, possibly due to the effects of 
      histologically observed ovarian toxicity. The nondioxin-like compounds, PCB 153 
      and 1,3,6,8-TCDD, produced no observable effects on endometriosis. Hepatic EROD 
      activity was significantly induced by 2,3,7,8-TCDD, 4-PeCDF, and PCB 126, but not 
      by PCB 153 or 1,3,6,8-TCDD. The results of this study provide preliminary support 
      for the hypothesis that halogenated aromatic hydrocarbon-promoted endometriosis 
      may be Ah receptor mediated.
FAU - Johnson, K L
AU  - Johnson KL
AD  - University of North Carolina, Chapel Hill 27599-7270, USA.
FAU - Cummings, A M
AU  - Cummings AM
FAU - Birnbaum, L S
AU  - Birnbaum LS
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Benzofurans)
RN  - 0 (Hydrocarbons, Halogenated)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - DFC2HB4I0K (Polychlorinated Biphenyls)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - Animals
MH  - Benzofurans/adverse effects/*pharmacology
MH  - Cytochrome P-450 CYP1A1/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Endometriosis/*chemically induced/physiopathology
MH  - Female
MH  - Hydrocarbons, Halogenated/adverse effects/*pharmacology
MH  - Liver/pathology
MH  - Mice
MH  - Ovary/pathology
MH  - Polychlorinated Biphenyls/adverse effects/*pharmacology
MH  - Polychlorinated Dibenzodioxins/adverse effects/*pharmacology
MH  - Structure-Activity Relationship
MH  - Uterus/pathology
PMC - PMC1470109
EDAT- 1997/07/01 00:00
MHDA- 1997/09/19 00:01
PMCR- 1997/07/01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/09/19 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
PHST- 1997/07/01 00:00 [pmc-release]
AID - 10.1289/ehp.97105750 [doi]
PST - ppublish
SO  - Environ Health Perspect. 1997 Jul;105(7):750-5. doi: 10.1289/ehp.97105750.