On the biosynthesis of ubiquinone (50)

Relationship Between Levels of Ubiquinones (Coenzymes Q) and Vitamin a in Livers of Australian Sheep and Cattle

“…Since this discovery, research in the field has progressed rapidly. The above observations and the fact that administration of vitamin A restored normal ubiquinone levels in the liver were confirmed by Gloor and Wiss (1959) and by many other workers as rcvicwed by Olson (1966) and Bieri (1966).…”

Biochemistry of Mitochondrial Coenzyme Q Biosynthesis

“…In mammals, the isoprene subunits for CoQ biosynthesis are generated through the mevalonate pathway [32, 44–46], stitched together by head-to-tail polymerization [47, 48], and attached to the head group via an electrophilic aromatic substitution [49] (Figure 2). The responsible prenyltransferases, Coq1p (PDSS1 and PDSS2) and Coq2p (COQ2) (see Glossary and Box 1 for “COQ” nomenclature) are localized to the inner mitochondrial membrane [25, 50–59], a key point marking the switch from cytosolic precursor generation to mitochondrial CoQ biosynthesis.…”

Effect of Retinol Feeding on Liver Cholesterol of Rats

“…Experiments of Heaton et al (1) and Gloor and Wiss (2,8) on the rate of incorporation of acetate-1-14C and mevalonate-2-14C into liver ubiquinone, squalene and cholesterol of vitamin A deficient rats suggested that vitamin A regulated the synthesis of cholesterol at squalene level. In vitamin A deficiency the incorpora tion of the label in ubiquinone and squalene was increased, whereas the incorpora tion of the label into cholesterol fraction was decreased (1, 2, 8).…”

“…Studies in hypo-and hypervitaminotic A rats have implicated the role of vitamin A in isoprene metabolism (1)(2)(3)(4)(5)(6)(7)(8)(9). Deficiency of vitamin A reduced the incorporation of acetate-1-14C, and mevalonate-2-14C into liver cholesterol, whereas excess of vitamin A caused an increased incorporation of acetate-1-14C and meva lonate-2-14C into liver cholesterol (1,2,8).…”

“…Deficiency of vitamin A reduced the incorporation of acetate-1-14C, and mevalonate-2-14C into liver cholesterol, whereas excess of vitamin A caused an increased incorporation of acetate-1-14C and meva lonate-2-14C into liver cholesterol (1,2,8). This shift in cholesterol metabolism due to vitamin A status of the animal has been implicated at the squalene level.…”