Alpha-decarboxylation, an important pathway for degradation of phytanic acid in animals.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
C E Mize
Publications and source records attributed to C E Mize.
Effects of dietary phytol and phytanic acid in animals.
Feeding of phytol in large doses (2-5% by weight in the diet) led to accumulation of phytanic acid in the mouse, rat, rabbit, and chinchilla, the degree of accumulation depending upon the level of dietary intake. The relative concentration of phytanic acid, expressed as a percentage of the total fatty acids, was as high as 20-60% in liver and 30-40% in serum. Phytenic acid, which may be an intermediate in the conversion of phytol to phytanic acid, also accumulated. When phytol was withdrawn from the diet, tissue and serum concentrations of phytanic acid fell rapidly, which indicates the ability of the normal animal to metabolize phytanic acid readily. At high dosages in the diet, phytol inhibited growth and caused death within 1-4 weeks. In the mouse, dietary phytanic acid and dietary phytol fed in equivalent amounts were of comparable toxicity. Accumulation of tissue phytanic acid occurred more rapidly when phytanic acid was fed than when phytol was fed in equal amounts. In none of the animals fed either phytol or phytanic acid were there any signs of neurological defects. Histologic examination of rats fed phytol showed some fat accumulation, glycogen depletion, and karyokinesis in the liver. There were no pathologic changes in the retina or in the peripheral and central nervous system such as those described in Refsum's disease.
Adrenal Glands↗
Metabolism of phytol-U-14C and phytanic acid-U-14C in the rat.
The metabolism of uniformly-labeled (14)C-phytol, (14)C-phytenic acid, and (14)C-phytanic acid was studied in the rat. Conversion of both phytol and phytenic acid to phytanic acid was demonstrated. Tracer doses of phytol-U-(14)C given orally were well absorbed (30-66%), and approximately 30% of the absorbed dose was converted to (14)CO(2) in 18 hr. After intravenous injection, 20% appeared in (14)CO(2) in 4 hr. Phytanic acid-U-(14)C given intravenously was oxidized at a comparable rate (22-37% in 4 hr) and was as rapidly oxidized as palmitic acid-1-(14)C (21% in 4 hr). Metabolism of these substrates was also studied in rats previously maintained on a diet containing 5% phytol by weight, which causes accumulation of phytanic acid, phytenic acid, and, to a lesser extent, phytol in blood and tissues. Despite the large body pools of preformed, unlabeled substrate in these animals, the fraction of an administered dose of phytol-U-(14)C or phytanic acid-U-(14)C converted to (14)CO(2) was not significantly diminished. These studies indicate that the rat has an appreciable capacity to degrade the highly branched carbon skeleton of phytol and its derivatives. Twenty-four hours after administration of phytol-U-(14)C, the lipid radioactivity remaining in the body was widely distributed among the tissues, highest concentrations being found in liver and adipose tissue. Four hours after intravenous administration of phytanic acid-U-(14)C, all of the major lipid classes in the liver contained radioactivity, most in triglycerides and phospholipids and least in cholesterol esters and lower glycerides. There was no demonstrable incorporation of mevalonate-2-(14)C or acetate-1-(14)C into liver phytanic acid when they were given intravenously to a rat previously fed phytol. Endogenous biosynthesis, if it occurs at all, must be extremely limited.
Adipose Tissue↗