Origin and Extrarenal Elimination of Uric Acid in Man

Sørensen, Leif; Levinson, Dennis J.

doi:10.1159/000180432

Cited by 126 publications

(67 citation statements)

References 14 publications

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“…In vitro studies of purine absorption in the hamster have shown that hypoxantine, xanthine and to a lesser extent uric acid are preferentially excreted rather than absorbed across the intestine (Berlin and Hawkins, 1968), while studies in sheep have indicated that the capacity of the small intestine to absorb allantoin is limited (Chen et al, 1990b). Nucleic acids, free bases (except xanthine) and PDs entering the large intestine do not appear to be absorbed due to extensive degradation by indigenous microbes (Sorensen, 1960;Ellis and Bleichner, 1969a;Chen et al, 1990a), and therefore purines excreted in faeces appear to be primarily derived from microbes residing in the caecum (Surra et al, 1997b). Furthermore, variations in the supply of NAs entering the caecum and the extent of hindgut fermentation do not appear to affect urinary PD excretion, but there is evidence to suggest that it is positively influenced by the flow of undigested fibre in the duodenum (Surra et al, 1997b).…”

Section: Digestion Of Nucleic Acidsmentioning

confidence: 99%

Estimation of microbial protein supply in ruminant animals based on renal and mammary purine metabolite excretion. A review

Shingfield¹

2000

J. Anim. Feed Sci.

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The potential of mammary and renal purine metabolite excretion as a technique for the assessment of microbial protein supply in ruminant animals is reviewed. Data reported in the literature tends to support the validity of the assumptions of the technique that purines entering the duodenum are essentially microbial in origin and that following metabolism, purine catabolites (collectively allantoin, hypoxanthine, uric acid and xanthine) are quantitatively recovered in urine. The most convincing experimental evidence suggests that secretion of purine metabolites in milk is of little value for the assessment of microbial protein supply due a mumal correlation with milk yield. In contrast, use of urinary purine metabolite excretion does appear to provide estimates of microbial protein supply that, are in general, consistent with values derived using standard in vivo procedures. However, the accuracy of this approach is largely dependent on obtaining representative samples of rumen microbes and the ability to account for variations in non-renal excretion and endogenous purine losses. In conclusion, urinary purine metabolite excretion appears to represent a valid noninvasive procedure to assess relative differences, rather than quantitative estimates of microbial protein supply in ruminant animals.

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Section: Digestion Of Nucleic Acidsmentioning

confidence: 99%

Estimation of microbial protein supply in ruminant animals based on renal and mammary purine metabolite excretion. A review

Shingfield¹

2000

J. Anim. Feed Sci.

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“…In adult humans approximately two-thirds of the uric acid is eliminated through the kidneys and one-third through the gastrointestinal tract (16). Renal handling of uric acid seems to involve four steps: glomerular filtration, tubular reabsorption, active secretion, and postsecretory reabsorption (17).…”

Section: Metabolismmentioning

confidence: 99%

Hypoxanthine as an Indicator of Hypoxia: Its Role in Health and Disease through Free Radical Production

Saugstad¹

1988

Pediatr Res

379

206

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Hypoxia is a common insult during the perinatal and neonatal period. New and better ways to evaluate hypoxia are needed. In 1975 we demonstrated high concentrations of the purine metabolite hypoxanthine in umbilical cord plasma after intrauterine hypoxia and proposed that hypoxanthine could be used as an indicator of hypoxia (1). Since then a large number of studies have been published dealing with different aspects of hypoxanthine in hypoxia. However, investigators in this field have encountered several methodologic problems: 1) Hypoxanthine leaks rapidly from erythrocytes (2, 3); if plasma is not separated promptly from red cells, falsely elevated plasma hypoxanthine concentrations will be found. 2) There are large variations in purine metabolism among species. 3) No clear definition of clinical hypoxia is available. Many authors do not distinguish between the terms hypoxemia and hypoxia, which adds to the confusion. We define tissue hypoxia as: "oxygen deficiency resulting in altered or interrupted energy metabolism" (4). It is important to be aware that hypoxia has two stages. In the first stage it is compensated because the cells are able to meet energy demands through anaerobic metabolism and other mechanisms. (We are not dealing with physiologic adaptation to hypoxia.) In the second stage of hypoxia or uncompensated hypoxia, energy demands are not met and cell injury ensues. At present there are no techniques for distinguishing between these two stages in clinical medicine, and such a distinction would be useful. Theoretically hypoxanthine should only be elevated in uncompensated hypoxia, while pH and lactate changes occur in compensated hypoxia. It seems, however, that hypoxanthine is also elevated to some extent in uncompensated hypoxia.Renewed interest in hypoxanthine developed when it was realized that hypoxanthine is a potential free radical generator (5, 6). Hypoxanthine seems to play a role in posthypoxic reoxygenation cell injury through oxygen radical production (7) and is therefore involved in the pathogenesis of a number of diseases. Hypoxanthine also modulates a number of other processes because it reacts with benzodiazepine receptors (8) and inhibits phosphodiesterase in the brain (9). Hypoxanthine inhibits the effect of several cytotoxic drugs and may therefore influence treatment with such drugs (10).Herein we summarize the extensive literature on hypoxanthine published during the last decade and try to answer the question: How useful in clinical medicine are hypoxanthine measurements in plasma and other body fluids? Is hypoxanthine a better marker of hypoxia than lactate or pH? Further, we discuss the significance of hypoxanthine as a potential oxygen radical generator and put forward a hypothesis for the pathogenesis of an "oxygen radical disease in neonatology". In hypoxia there is an accelerated breakdown of AMP to hypoxanthine. Figure 1 illustrates several important aspects of hypoxanthine metabolism in hypoxia. Normally about 90% of the hypoxanthine formed is reutilized through the sa...

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“…The magnitude of purine loss can be between 5% and 9% of the resting muscle ATP content (Bangsbo et al 1992;Hellsten et al 1999). It has been reported that the plasma purines are excreted in the urine (Nasrallah and Al Khalidi 1964;Sutton et al 1980;Stathis et al 1999), or converted to uric acid (Hellsten et al 1994) and subsequently excreted (Nasrallah and Al Khalidi 1964;Sorensen and Levinson 1975;Stathis et al 1999). Sorensen and Levison (1975) demonstrated that, in a resting individual, the uric acid loss via the gut is one third, whilst via the urine is two thirds of the total uric acid loss in the untrained individual.…”

Section: Introductionmentioning

confidence: 99%

Sprint training reduces urinary purine loss following intense exercise in humans

Stathis

Carey

Hayes

et al. 2006

Appl. Physiol. Nutr. Metab.

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The influence of sprint training on endogenous urinary purine loss was examined in seven active male subjects (age: 23.1 ± 1.8 years, weight: 76.1 ± 3.1 kg, VO 2 peak:56.3 ± 4.0 ml.kg -1 .min -1 ). Each subject performed a 30s sprint performance test (PT), before and after 7 days of sprint training. Training consisted of fifteen 10s sprints on an air-braked cycle ergometer performed twice per day. A rest period of 50s separated each sprint during training. Sprint training resulted in a 20% higher muscle ATP immediately after PT, a lower IMP (57% and 89%, immediately following and after 10 min recovery from PT, respectively), and inosine accumulation (53% and 56%, immediately following and 10 min after the PT, respectively). Sprint training also attenuated the exercise-induced increases in plasma inosine, hypoxanthine (Hx) and uric acid during the first 120 min of recovery and reduced the total urinary excretion of purines (inosine + Hx + uric acid) in the 24 hours recovery following intense exercise. These results show that intermittent sprint training reduces the total urinary purine excretion after a 30s sprint bout.

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Origin and Extrarenal Elimination of Uric Acid in Man

Cited by 126 publications

References 14 publications

Estimation of microbial protein supply in ruminant animals based on renal and mammary purine metabolite excretion. A review

Estimation of microbial protein supply in ruminant animals based on renal and mammary purine metabolite excretion. A review

Hypoxanthine as an Indicator of Hypoxia: Its Role in Health and Disease through Free Radical Production

Sprint training reduces urinary purine loss following intense exercise in humans

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