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- W2133887528 abstract "The serum level of α1-acid glycoprotein (α1-AGP) is significantly increased in various animal species by treatment with cytokines, glucocorticoids and phenobarbital. The mechanisms responsible for the cytokine-induced and glucocorticoid-induced increases are now well documented, but not so in the case of phenobarbital. The main purpose of this study was to assess whether phenobarbital acts on α1-AGP synthesis in the liver at the transcriptional or translational level. Male Dark Agouti rats received 70 mg phenobarbital/kg daily for 7 days. The analysis of total hepatic RNA showed that a single injection of phenobarbital induced an 11-fold increase in phenobarbital-dependent cytochrome P450IIB mRNA, whereas seven injections of phenobarbital were required to induce a maximum 5.5-fold increase in α1-AGP mRNA. Concurrently, the transcription rate of the α1-AGP gene rose 3.5-fold. Hepatocytes isolated after the seventh injection of phenobarbital showed a threefold increased capacity to secrete α1-AGP, corresponding to a 3.2-fold increased α1-AGP mRNA content in the liver. In conditions in which its effect on the induction of α1-AGP synthesis was maximum, phenobarbital caused a 30 % reduction in liver albumin mRNA and in albumin secretion by isolated hepatocytes, resulting from a 60–70 % reduction in the rate of transcription of the albumin gene measured in isolated nuclei. We conclude that the effect of phenobarbital on α1-AGP and albumin gene expression occurs at the transcriptional rather than the translational level." @default.
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- W2133887528 date "1992-02-01" @default.
- W2133887528 modified "2023-10-18" @default.
- W2133887528 title "Modifications of hepatic alpha-1-acid glycoprotein and albumin gene expression in rats treated with phenobarbital" @default.
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- W2133887528 doi "https://doi.org/10.1111/j.1432-1033.1992.tb16595.x" @default.
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