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Cloning of a cDNA coding for P-450 LM3c from rabbit liver microsomes and regulation of its expression

Nucleic Acids Research
|August 11, 1986
PubMed

Insights

Macrolide antibiotics like triacetyloleandomycin (TAO) increase rabbit liver cytochrome P-450 LM3c protein levels significantly. This induction appears to occur via post-transcriptional effects, not increased gene transcription.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Cytochromes P-450 (CYPs) are crucial enzymes in drug metabolism.
  • Liver CYPs LM3c (rabbit) and P-450p (rat) are related, inducible forms.
  • Induction is triggered by macrolide antibiotics and glucocorticoids.

Purpose of the Study:

  • To investigate the mechanism of cytochrome P-450 LM3c induction by TAO.
  • To characterize the cDNA for rabbit liver cytochrome P-450 LM3c.
  • To determine if induction involves transcriptional or post-transcriptional regulation.

Main Methods:

  • Preparation of a cDNA library from TAO-induced rabbit liver mRNA.
  • Characterization of LM3c cDNA (pLM3c-4.1) and hybridization studies.
  • Northern blot analysis of liver poly(A)RNA from treated and untreated rabbits.
  • Measurement of P-450 LM3c gene transcription rates in isolated liver nuclei.

Main Results:

  • A cDNA (pLM3c-4.1) for LM3c was identified and hybridized with a P-450p cDNA probe.
  • Northern blots revealed two mRNA species (~1700 and ~1850 nucleotides) that hybridized to LM3c cDNA.
  • Macrolide antibiotics increased both mRNA species fivefold, while phenobarbital and B-naphthoflavone had no effect.
  • LM3c protein increased 25-fold after 5 days of TAO treatment, while mRNA increased only fivefold.
  • Gene transcription rates remained unchanged during TAO treatment.

Conclusions:

  • Triacetyloleandomycin (TAO) induces cytochrome P-450 LM3c protein in rabbit liver.
  • The induction mechanism involves post-transcriptional regulation rather than increased gene transcription.
  • This study elucidates a key regulatory pathway for drug-metabolizing enzymes.

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