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The regulation of the biosynthesis of ubiquinone in the rat.

Abstract
The urinary excretion of p-hydroxybenzoate was not altered by ubiquinone feeding, but, although decreased considerably, was not eliminated in protein deficiency. The incorporation of p-hydroxy[U-14C]benzaldehyde into ubiquinone in vivo increased in cold-exposed and p-chlorophenoxyisobutyrate (clofibrate)-fed rats, and these changes were parallel with the changes in the incorporation of [2-14C]mevalonate under these conditions. Starvation, cholesterol feeding and cholic acid feeding resulted in the decreased incorporation of p-hydroxy[U-14C]benzaldehyde into ubiquinone, confirming the decreased ubiquinone synthesis. Feeding exogenous ubiquinone increased the hepatic ubiquinone concentration, but did not cause any decrease in the incorporation of p-hydroxy[U-14C]benzaldehyde into ubiquinone, indicating the absence of a feedback control.
AuthorsS Ranganathan, T Ramasarma
JournalThe Biochemical journal (Biochem J) Vol. 148 Issue 1 Pg. 35-9 (Apr 1975) ISSN: 0264-6021 [Print] England
PMID1156398 (Publication Type: Journal Article)
Chemical References
  • Benzaldehydes
  • Hydroxybenzoates
  • Ubiquinone
  • Clofibrate
  • Mevalonic Acid
Topics
  • Animals
  • Benzaldehydes (metabolism)
  • Clofibrate (pharmacology)
  • Cold Temperature
  • Feedback
  • Hydroxybenzoates (urine)
  • In Vitro Techniques
  • Liver (metabolism)
  • Male
  • Mevalonic Acid (metabolism)
  • Protein Deficiency (metabolism)
  • Rats
  • Ubiquinone (biosynthesis)

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