Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 342, Issue 4, Pages 1375-1381Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2006.02.121
Keywords
aromatic hydrocarbon receptor; cytochrome P450; liver; mitochondria; mice; oxidative stress; TCDD
Categories
Funding
- NIEHS NIH HHS [P30 ES06096, R01 ES10133, R01 ES08799, R01 ES12463, T32 ES07250, R01 ES08147] Funding Source: Medline
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TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) induces cytochromes P450 (CYPs) such as CYP1A1 and CYP1A2 via activation of the aromatic hydrocarbon receptor (AHR). Herein we describe the TCDD-dependent enrichment of CYPs in liver microsomes and mitoplasts from C57BL/6J mice. TCDD-induced accumalation of CYP1A1 and CYP1A2 was observed in microsomes and mitoplasts after treatment with 15 mu g TCDD/kg/d for 3 d. While microsomal CYP1 proteins peaked at 1 week and diminished thereafter, mitoplast CYP1 proteins persisted 8 weeks at high levels. TCDD also induced microsomal CYP2A5, but not microsomal proteins immunoreactive to CYP2C11, CYP3A2 or CYP4A1 antibodies. Nevertheless, each of these proteins increased in mitoplasts following TCDD exposure. These results suggest that TCDD increases mitochondrial CYP immunoreactive proteins Under the transcriptional control of the AHR, as well as CYPs that are not Under AHR control. We speculate that such mitochondrial CYPs may be involved in the generation, or mitigation, of the well-known TCDD-inducible oxidative stress response. (c) 2006 Elsevier Inc. All rights reserved.
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