Superinduction of 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible expression of aldehyde dehydrogenase by the inhibition of protein synthesis.
Inhibition of protein synthesis by cycloheximide or puromycin super-induced the 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible isoform of aldehyde dehydrogenase (ALDH-3) in rat hepatoma cells. Treatment with cycloheximide did not affect the basal expression but markedly enhanced the TCDD-inducible expression of ALDH-3 mRNA. The co-treatment of cycloheximide and TCDD for 24 h caused a 10-fold greater accumulation of ALDH-3 mRNA than did TCDD alone. The transcription rate of the ALDH-3 gene in the co-treated cells was also 4- to 5-fold higher than that in the cells treated with TCDD alone. The superinduction of ALDH-3 mRNA was observed only when cycloheximide was added prior to or simultaneously with the addition of TCDD. These results suggest that the mechanism of TCDD-inducible transcription of the ALDH-3 gene involves a labile protein that modulates or represses the action of TCDD.
Takimoto
K
K
McArdle Laboratory for Cancer Research, Department of Oncology, Medical School, University of Wisconsin, Madison 53706.
Lindahl
R
R
Pitot
H C
HC
D000199:Actins / Q000235:genetics; D000444:Aldehyde Dehydrogenase / Q000096:biosynthesis / Q000235:genetics*; D000818:Animals; D015152:Blotting, Northern; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D007527:Isoenzymes / Q000096:biosynthesis / Q000235:genetics*; D007700:Kinetics; D008114:Liver Neoplasms, Experimental; D000072317:Polychlorinated Dibenzodioxins / Q000494:pharmacology*; D011691:Puromycin / Q000494:pharmacology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics*; D051381:Rats; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects*
D000199:Actins; D007527:Isoenzymes; D000072317:Polychlorinated Dibenzodioxins; D012333:RNA, Messenger; D011691:Puromycin; D003513:Cycloheximide; D000444:Aldehyde Dehydrogenase