Biosynthesis of ubiquinone‐9 was studied by incubating rat liver mitochondria with p‐hydroxy[U‐14C]benzoate, solanesyl diphosphate and S‐adenosyl‐l‐methionine. When methylation reactions were inhibited by replacing S‐adenosyl‐l‐methionine with S‐adenosyl‐l‐homocysteine, nonaprenyl p‐hydroxybenzoate and three other labeled peaks, designated as P1, P2 and P3 according to their retention times on HPLC, were observed. No carboxyl group was present in P1, P2 or P3 because the radioactivities disappeared when p‐hydroxy[U‐14C]benzoate was replaced by p‐hydroxy[carboxyl‐14C]benzoate. Compound P2 seemed to be hydroxylated but not methylated because its radioactivity markedly diminished under anaerobic conditions and the radioactivity was not incorporated into the compound from S‐adenosyl‐l‐[methyl‐3H]methionine, suggesting that P2 is 6‐hydroxynonaprenylphenol. The complete correspondence of the retention times of P2 and chemically synthesized 6‐hydroxynonaprenylphenol on HPLC further confirmed this possibility. P2 was a precursor of ubiquinone‐9 because the radioactivity of the compound was incorporated into ubiquinone when incubated with mitochondria. The results suggest that the decarboxylation may occur prior to the first methylation in the ubiquinone biosynthesis in rat liver mitochondria, though it has been generally considered that in eukaryotes the first methylation precedes the decarboxylation.
|Number of pages||7|
|Journal||European Journal of Biochemistry|
|Publication status||Published - Jun 1991|
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