scholarly journals Comparative Study on the Nuclear Hormone Receptor Activity of Various Phytochemicals and Their Metabolites by Reporter Gene Assays Using Chinese Hamster Ovary Cells

2009 ◽  
Vol 32 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Shinji Takeuchi ◽  
Tetsuo Takahashi ◽  
Yukiharu Sawada ◽  
Mitsuru Iida ◽  
Tadashi Matsuda ◽  
...  
Keyword(s):  
Comparative Study ◽  
Reporter Gene ◽  
Chinese Hamster Ovary ◽  
Hormone Receptor ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Nuclear Hormone Receptor ◽  
Receptor Activity ◽  
Ovary Cells ◽  
Reporter Gene Assays

Pre-UV-Treatment of Cells Results in Enhanced Host Cell Reactivation of a UV Damaged Reporter Gene in CHO-AA8 Chinese Hamster Ovary Cells but Not in Transcription-Coupled Repair Deficient CHO-UV61 Cells

2004 ◽  
Vol 24 (6) ◽  
pp. 559-576 ◽  
Author(s):  
Lili Liu ◽  
Andrew J. Rainbow
Keyword(s):  
Host Cell ◽  
Reporter Gene ◽  
Chinese Hamster Ovary ◽  
Excision Repair ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Ovary Cells ◽  
Cell Reactivation ◽  
Host Cell Reactivation ◽  
Transcription Coupled Repair

We have used a non-replicating recombinant adenovirus, Ad5MCMVlacZ, which expresses the β-galactosidase reporter gene, to examine both constitutive and inducible repair of UV-damaged DNA in repair proficient CHO-AA8 Chinese hamster ovary cells and in mutant CHO-UV61 cells which are deficient in the transcription-coupled repair (TCR) pathway of nucleotide excision repair. Host cell reactivation (HCR) of β-galactosidase activity for UV-irradiated Ad5MCMVlacZ was significantly reduced in non-irradiated CHO-UV61 cells compared to that in non-irradiated CHO-AA8 cells suggesting that repair in the transcribed strand of the UV-damaged reporter gene in untreated cells utilizes TCR. Prior UV-irradiation of cells with low UV fluences resulted in a transient enhancement of HCR for expression of the UV-damaged reporter gene in CHO-AA8 cells but not in TCR deficient CHO-UV61 cells. These results suggest the presence of an inducible DNA pathway in CHO cells that results from an enhancement of TCR or a mechanism that involves the TCR pathway.

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