[Induction of aryl hydrocarbon receptor and CYP1A1 mRNA by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver].
OBJECTIVE
To explore the toxic mechanism of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) by studying the induction of cytochrome P4501A1 (CYP1A1) and aryl hydrocarbon receptor (AHR) mRNA in liver of TCDD-treated SD rats.


METHODS
Thirty female SD rats were randomly divided into control group and 5 exposure groups, every group had 5 rats. The animals were treated i.p. with 0.01, 0.1, 1, 10, 50 microg TCDD/kg BW. AHR and CYP1A1 mRNA expression were analyzed by RT-PCR after 24 h.


RESULTS
The contents of AHR and CYP1A1 mRNA were increased in all exposure groups except the 0.01 microg TCDD/kg BW group. AHR mRNA content was significantly increased in 50 microg TCDD/kg BW group (P<0.05); CYP1A1 mRNA contents were significantly increased in all exposure groups (P<0.05) but not 0.01 microg TCDD/kg BW group. There were dose-response relationship between TCDD doses and AHR, CYP1A1 gene expression.


CONCLUSIONS
Both AHR and CYP1A1 gene in liver of TCDD-treated SD rats can be induced 24 h after exposure and CYP1A1 gene is more inducible than AHR gene.
Liu
Yun-ru
YR
School of Public Health, Tianjin Medical University, Tianjin 300070, China.
Tang
Nai-jun
NJ
Ren
Da-lin
DL
D000818:Animals; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics*
D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon; D019363:Cytochrome P-450 CYP1A1