Induction of aryl hydrocarbon receptor and CYP1A1 mRNA by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat liver.
- Author:
Yun-ru LIU
1
;
Nai-jun TANG
;
Da-lin REN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cytochrome P-450 CYP1A1; genetics; Dose-Response Relationship, Drug; Female; Gene Expression Regulation; drug effects; Liver; drug effects; metabolism; Polychlorinated Dibenzodioxins; toxicity; Rats; Rats, Sprague-Dawley; Receptors, Aryl Hydrocarbon; genetics
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2003;21(6):417-419
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSThirty 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.
RESULTSThe 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.
CONCLUSIONBoth 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.
