Pyridoxic acid excretion

Cohurn SP, Thampy KG, Lane HW, Conn PS, Ziegler PJ, Costill DL, Mahuren JD, Fink WJ, Pearson DR, Schaltenhrand WE, et al. (1995) Pyridoxic acid excretion during low vitamin B-6 intake, total fasting, and hed rest. American Joumai ofCiinicai Nutrition 62,979-83. 

As noted earlier, our data suggested that a 50% decrease in pyridoxal concentration might result in a 90% decrease in pyridoxic acid excretion (Cobum et ai, 1991). The pyridoxal data suggested that the maximum pool... 

K Schuster, LB Bailey, JJ Cerda, JF Gregory. Urinary 4-pyridoxic acid excretion in 24-hour versus random urine samples as a measurement of vitamin B status in humans. Am J Chn Nutr 39 466-470, 1984. 

Although, owing to the wide distribution of vitamin Bg in nature, clinical deficiency symptoms are seldom observed, there is little doubt that pyridoxine is essential in human nutrition. Pyridoxine is absorbed from the gastrointestinal tract and is converted to the active form pyri-doxal phosphate. Absorption is decreased in gastrointestinal diseases and also in subjects taking isoniazid (3). It is excreted in the urine as 4-pyridoxic acid (2). The metabolism of vitamin Bg in human beings has been investigated (56). 

Moller (57) has recognized pyridoxine, pyridoxal, pyridoxa-mine, and 4-pyridoxic acid as the excretion products of vitamin Bg. Complete balance studies have been made in pigs and in babies on all the known vitamin Bg metabolic compounds. In babies, the total output exceeded the intake. The assumption that a limited synthesis of vitamin Bg occurs seems justifiable. 

Free pyridoxal either leaves the cells or is oxidized to 4-pyridoxic acid by aldehyde dehydrogenase (which is present in all tissues) and also by hepatic and renal aldehyde oxidases. 4-Pyridoxic acid is actively secreted by the renal tubules, so measurement of the plasma concentration provides an index of renal function (Coburn et al., 2002). There is some evidence that oxidation to 4-pyridoxic acid increases with increasing age in elderly people, the plasma concentration of pyridoxal phosphate is lower, and that of 4-pyridoxic acid higher, than in younger subjects even when there is no evidence of impaired renal function (Bates et al., 1999b). Small amounts of pyridoxal and pyridox-amine are also excreted in the urine, although much of the active vitamin Be that is filtered in the glomerulus is reabsorbed in the kidney tubules. 

Muscle pyridoxal phosphate is released into the circulation (as pyridoxal) in starvation as muscle glycogen reserves are exhausted and there is less requirement for glycogen phosphorylase activity. Under these conditions, it is potentially available for redistribution to other tissues, especially the liver and kidneys, to meet the increased requirement for gluconeogenesis from amino acids (Black et al., 1978). However, during both starvation and prolonged bed rest, there is a considerable increase in urinary excretion of 4-pyridoxic acid, suggesting that much of the vitamin Be released as a result of depletion of muscle glycogen and atrophy of muscle is not redistributed, but rather is ca-tabolized and excreted (Cobum et al., 1995). 

As shown in Table 9.5, there are a number of indices of vitamin Be status available plasma concentrations of the vitamin, urinary excretion of 4-pyridoxic acid, activation of erythrocyte aminotransferases by pyridoxal phosphate added in vitro, and the ability to metabolize test doses of tryptophan and methionine. None is wholly satisfactory and where more than one index has been used in population studies, there is poor agreement between the different methods (Bender, 1989b Bates et al., 1999a). 

About half of the normal dietary intake of vitamin Be is excreted as 4-pyridoxic acid (see Figure 9.1). Urinary excretion of 4-pyridoxic acid will largely reflect recent intake of the vitamin rather than underlying nutritional status. More importantly, renal clearance of 4-pyridoxic acid is a marker of renal function, irrespective of vitamin Be status (Bates et al., 1999a Coburn et al., 2002). 

Early studies of vitamin Be requirements used the development of abnormalities of tryptophan or methionine metabolism during depletion, and normalization during repletion with graded intakes of the vitamin. Although tryptophan and methionine load tests are unreliable as indices of vitamin Be status in epidemiological studies (Section 9.5.4 and Section 9.5.5), under the controlled conditions of depletion/repletion studies they do give a useful indication of the state of vitamin Be nutrition. More recent studies have used more sensitive indices of status, including the plasma concentration of pyridoxal phosphate, urinary excretion of 4-pyridoxic acid, and erythrocyte transaminase activation coefficient. 

Disposition in the Body. Absorbed from the gastro-intestinal tract and converted to the active form, pyridoxal phosphate. Excreted in the urine mainly as 4-pyridoxic acid. 

Aksenova and Messineva (A2) investigated the excretion of 4-pyridoxic acid in 63 patients affected by different forms of leukemia and hypoplastic anemia. Since all pyridoxine derivatives are oxidized to 4-pyridoxic acid, such a compound was considered an index of vitamin Be balance. These patients showed a deficiency of pyridoxine, which increased with simultaneous loadings of tryptophan and pyridoxine (A2). 

Gershoff and Prien (G6) found that normal subjects excrete significantly less xanthurenic acid and 4-pyridoxic acid and more citric acid than patients with chronic formation of calcium oxalate. A marked rise in excretion of calcium oxalate followed administration of tryptophan in these patients, whereas ingestion of pyridoxine was followed by a decrease in urinary oxalate. 

Several tests are available for asses ing vitamin B status measurement of plasma levels of PLP, measurement of the percentage stimulation of red blood cell glula-matc-oxaloacetate aminotransferase, measurement of the daily excretion of urinary pyridoxic acid, and the tryptophan load test. 

Most of the vitamin in the body is eventually degraded to pyridoxic acid (PX) and excreted in the urine. Vitamin deficiency can result in a decrease in the amount of PX excreted, as illustrated by the data tn Table 9.4. Human subjects who had consumed a B i-sufficient diet were fed a B(,-deficient diet for 45 days. The results... 

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