Characterization of the Ah Receptor Mediating Aryl Hydrocarbon Hydroxylase Induction in the Human Liver Cell Line Hep G2

Roberts, EA; Johnson, KC; Harper, PA; Okey, AB

HERO ID

2136796

Reference Type

Journal Article

Year

1990

Language

English

PMID

2154949

HERO ID 2136796
In Press No
Year 1990
Title Characterization of the Ah Receptor Mediating Aryl Hydrocarbon Hydroxylase Induction in the Human Liver Cell Line Hep G2
Authors Roberts, EA; Johnson, KC; Harper, PA; Okey, AB
Journal Archives of Biochemistry and Biophysics
Volume 276
Issue 2
Page Numbers 442-450
Abstract Ah receptor properties in human liver cells were examined. Sucrose gradient analysis was conducted by incubating 500 microliters of cytosolic preparations of human liver cell Hep-G2 with 10 nanomolar tritium labeled 2,3,7,8-tetrachlorodibenzo-p-dioxin (1746016) (TCDD) for 1 hour. Competitors included TCDD, 2,3,7,8-tetrachlorodibenzofuran (51207319) (TCDF), 2,3,4,7,8-pentachlorodibenzofuran (57117314) (PCDF), 3-methylcholanthrene (56495) (MC), and dibenzo(a,h)anthracene (53703) (DBahA). Radioactivity in fractions collected from the gradient was determined by liquid scintillation counting. Nuclear translocation was assessed and aryl-hydrocarbon-hydroxylase (AHH) activity was measured with and without preincubation with benz(a)anthracene (BA) or MC. Mouse Hepa-1 cells were used for comparison. The concentration of Ah receptor binding sites for TCDD in Hep-G2 cells was 112 femtomoles per milligram (fmol/mg). The concentration in Hepa-1 cells was 422fmol/mg. In Hep-G2 cells, the TCDDh receptor complex sedimented at 9S on sucrose density gradients. TCDD/Ah receptor binding was completely inhibited by TCDF, PCDF, MC, and DBahA. Phenobarbital (50066), dexamethasone (50022), and estradiol (50282) had no effect. The dissociation constant for the TCDD/Ah receptor complex was 9 nanomolar by Wolf plot analysis; this value was about an order of magnitude weaker than that seen using Hepa-1 cells. Cytosolic and nuclear TCDD/Ah receptor complexes that sedimented at 9S and 6S, respectively, were detected after incubation of whole Hep-G2 cells. 3MC and BA induced AHH activity in Hep-G2 cells in a dose dependent manner. The concentrations causing half maximal induction (EC50s) were 1.3 and 5.3 micromolar (microM), respectively. The EC50 for induction of AHH activity by BAin Hepa-1 cells was 0.3microM. The authors conclude that Hep-G2 cells possess a drug metabolizing activity that is associated with cytochrome-P-450IA1 and at least part of the receptor mechanism needed to regulate it.
Doi 10.1016/0003-9861(90)90743-i
Pmid 2154949
Wosid WOS:A1990CN60200021
Is Certified Translation No
Dupe Override No
Comments Scopus URL: https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025159425&doi=10.1016%2f0003-9861%2890%2990743-I&partnerID=40&md5=60ef72d68aa8df91dc2ce486607f5226
Is Public Yes
Language Text English