PMID- 14687977
OWN - NLM
STAT- MEDLINE
DCOM- 20040305
LR  - 20191108
IS  - 0166-445X (Print)
IS  - 0166-445X (Linking)
VI  - 66
IP  - 1
DP  - 2004 Jan 7
TI  - Histological analysis of acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin 
      (TCDD) in zebrafish.
PG  - 25-38
AB  - Previous studies have demonstrated that acute exposure to 
      2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by injection leads to inhibition of 
      caudal fin regeneration in zebrafish. Since the TCDD exposure in these studies is 
      systemic, it is possible that pathology in organs other than the fin could result 
      in inhibition of fin regeneration. Therefore, histopathology of adult zebrafish 
      (Danio rerio) organs was characterized following abdominal cavity injection of a 
      TCDD dose (70ng/g). The most pronounced histopathologic changes 5 days 
      post-injection included lipidosis and hypertrophy of liver hepatocytes and 
      hypertrophy of gill lamellae. Effects of TCDD exposure on immunolocalization of 
      the zebrafish aryl hydrocarbon receptor nuclear translocator (ARNT2), the 
      heterodimer partner of the aryl hydrocarbon receptor (AHR2), and an AHR regulated 
      gene cytochrome P450 1A (CYP1A) was also determined. ARNT2 was immunolocalized to 
      the gastrointestinal tract, gill lamellae, kidney, ventricle of the heart, caudal 
      fin, brain and liver of zebrafish. TCDD exposure had no measurable effect on 
      ARNT2 abundance or localization. CYP1A was immunolocalized in TCDD exposed fish 
      as a biomarker for cells with an activated AHR pathway. CYP1A was not detected in 
      any tissue from vehicle exposed fish. Significant TCDD-dependent induction of 
      CYP1A was detected in the proximal tubules of the kidney, in liver hepatocytes 
      and in the gastrointestinal tract of TCDD exposed fish. Significant but lower 
      TCDD-dependent CYP1A expression was evident in the gill, caudal fin and ventricle 
      of the heart. Overall, TCDD exposure in adult zebrafish leads to histopathology 
      similar to that reported in other fish species, and it appears unlikely that the 
      histopathology in these organs completely explains the inhibition of fin 
      regeneration.
FAU - Zodrow, Jeanmarie M
AU  - Zodrow JM
AD  - Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado 
      Health Sciences Center, Denver 80262, USA.
FAU - Stegeman, John J
AU  - Stegeman JJ
FAU - Tanguay, Robert L
AU  - Tanguay RL
LA  - eng
GR  - R01 ES010820/ES/NIEHS NIH HHS/United States
GR  - ES10820/ES/NIEHS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Aquat Toxicol
JT  - Aquatic toxicology (Amsterdam, Netherlands)
JID - 8500246
RN  - 0 (AHR2 protein, zebrafish)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Polychlorinated Dibenzodioxins)
RN  - 0 (Receptors, Aryl Hydrocarbon)
RN  - 0 (Transcription Factors)
RN  - 0 (Zebrafish Proteins)
RN  - 0 (arnt2 protein, zebrafish)
RN  - 138391-32-9 (Aryl Hydrocarbon Receptor Nuclear Translocator)
RN  - 9035-51-2 (Cytochrome P-450 Enzyme System)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
SB  - IM
MH  - Animals
MH  - Aryl Hydrocarbon Receptor Nuclear Translocator
MH  - Cytochrome P-450 CYP1A1/*metabolism
MH  - Cytochrome P-450 Enzyme System/drug effects/genetics
MH  - Environmental Pollutants/*toxicity
MH  - Gills/*drug effects/pathology
MH  - Hepatocytes/*drug effects/pathology
MH  - Immunohistochemistry
MH  - Organ Specificity
MH  - Polychlorinated Dibenzodioxins/*toxicity
MH  - Receptors, Aryl Hydrocarbon/metabolism
MH  - Toxicity Tests, Acute
MH  - Transcription Factors/metabolism
MH  - Zebrafish/anatomy & histology/genetics/*metabolism
MH  - Zebrafish Proteins/metabolism
EDAT- 2003/12/23 05:00
MHDA- 2004/03/06 05:00
CRDT- 2003/12/23 05:00
PHST- 2003/12/23 05:00 [pubmed]
PHST- 2004/03/06 05:00 [medline]
PHST- 2003/12/23 05:00 [entrez]
AID - S0166445X03001760 [pii]
AID - 10.1016/j.aquatox.2003.07.002 [doi]
PST - ppublish
SO  - Aquat Toxicol. 2004 Jan 7;66(1):25-38. doi: 10.1016/j.aquatox.2003.07.002.