Purine Catabolism: Links to Mitochondrial Respiration and Antioxidant Defenses?

Kristal, Bruce S.; Vigneau-Callahan, Karen E.; Moskowitz, Alison J.; Matson, Wayne R.

doi:10.1006/abbi.1999.1387

Cited by 61 publications

(46 citation statements)

References 31 publications

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“…While the findings do indicate alterations in purine metabolism, it appears that some metabolic pathways (e.g., adenine and inosine to xanthine) showed reduced catabolism, while others (e.g., xanthine to guanine and guanine to guanosine) showed enhanced catabolism. Such pattern of accumulation of certain purine metabolites and elimination of others is typical of chronic disease states, such as diabetes, gout, schizophrenia, epilepsy, and chronic kidney disease (Kristal et al 1999;Lara et al 2006;Puig et al 1994;Vianna et al 2002). There are suggestions that the purine metabolites may be involved in oxidative-stress-related toxicity of cocaine to the brain and heart (Kovacic 2005).…”

Section: Alterations In Purine Metabolismmentioning

confidence: 96%

Alterations in tryptophan and purine metabolism in cocaine addiction: a metabolomic study

et al. 2009

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Section: Alterations In Purine Metabolismmentioning

confidence: 96%

Alterations in tryptophan and purine metabolism in cocaine addiction: a metabolomic study

et al. 2009

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“…Sera were aliquoted (125 lL) into microcentrifuge tubes and frozen in liquid nitrogen. For analysis, samples were thawed and proteins removed by acetonitrile extraction, and subjected to HPLC analysis coupled with coulometric array detection as previously described (Matson et al, 1984(Matson et al, , 1987Beal et al, 1990Beal et al, , 1992LeWitt et al, 1992;Ogawa et al, 1992;Milbury, 1997;Kristal et al, 1998Kristal et al, , 1999Shi et al, 2002a). Specifically, 500 lL of acetonitrile (An)/ 0.4% glacial acetic acid (HAc) was added to sera at )20°C; the samples were vortexed for 20 s, and then centrifuged 15 min/12000g at )2°C.…”

Section: Serum Preparationmentioning

confidence: 99%

Relative contribution of specific sources of systematic errors and analytical imprecision to metabolite analysis by HPLC–ECD

et al. 2005

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Objective interpretation of metabolomics data requires understanding both analytical and biological measurement errors. Here we address analytical measurement errors, the sources of these errors, and how this variability can impact metabolomic profiles. Sources considered include room temperature exposure (which could affect sample stability), spiking with authentic standards, the number of study replicates, the overall temporal design of the experimental series, and the complexity of the biological matrix of the samples (individual or pooled sera). The study focused on the analysis of $80 rat sera metabolites by HPLC coupled with coulometric array detectors. Time delay and room temperature exposure had minimal effects on the total relative metabolite concentrations and variability (mean: $94-98% of control, CV median : ±5-7%), but the concentrations of some specific metabolites were significantly altered. Changes observed in the concentrations of specific metabolites ranged as high as ±7-fold, with changes in variability ranging from 0.3% to 68%. Spiked samples demonstrated more complex behavior when allowed to decay over time than did control samples. The spiking of sera and standards with 43 known metabolites increased variability of the apparent concentrations of metabolites up to $24% as opposed to $3% in pure sera. Increased variability was metabolite-specific. In both pure and spiked sera, $80-95% of metabolites had CVs equivalent to standard analytical CVs for these metabolites. Experimental design, number of replicates, and complexity of the biological matrix had comparable effects. These results suggest that, under carefully controlled conditions, these analytical issues are not significant sources of variability relative to biological variation for most metabolites.

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“…Methionine residues, probably including ND2-237Met, act as endogenous antioxidants (Levine et al 1996). Moreover, purine catabolism, of which the final product is uric acid, provides a homeostatic mechanism to protect mitochondria from ROS (Kristal et al 1999). One possible mechanism is the biophysical and biochemical differences in the generation of ROS and/or in the sensitivity to ROS between ND2-237Leu and ND2-237Met.…”

Section: Discussionmentioning

confidence: 99%

Longevity-associated NADH dehydrogenase subunit-2 237 Leu/Met polymorphism influences the effects of alcohol consumption on serum uric acid levels in nonobese Japanese men

et al. 2006

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NADH dehydrogenase subunit-2 237 leucine/methionine (ND2-237 Leu/Met) polymorphism is reportedly associated with longevity in the Japanese population. The ND2-237Met genotype may confer resistance to cardiovascular and cerebrovascular atherogenic diseases. Hyperuricemia is one of the risk factors for cardiovascular disease. To investigate whether ND2-237 Leu/Met polymorphism is associated with serum uric acid (SUA) levels, we conducted a cross-sectional study in 321 healthy Japanese male subjects. In nonobese (body mass index, BMI < 25) male subjects, interaction between ND2-237 Leu/Met genotypes and drinking frequency on SUA levels was observed (P=0.031). The SUA levels were significantly higher in daily drinkers with ND2-237Leu than in non-daily drinkers with ND2-237Leu (P=0.018). In nonobese men, after adjustment for covariates, daily drinkers with ND2-237Leu had a significantly higher odds ratio (OR) for hyperuricemia (SUA ‡6.5 mg/dl: vs. daily drinkers with ND2-237Met, OR=3.26, 95% confidence interval (CI) 1.14-9.29; vs. non-daily drinkers with ND2-237Leu, OR=3.22, 95% CI 1.39-7.45; SUA ‡7.0 mg/dl: vs. non-daily drinkers with ND2-237Met, OR=3.53, 95% CI 1.00-12.4). However, in obese (BMI ‡25) men, no significant interaction between ND2-237 Leu/Met polymorphism and habitual drinking on SUA levels or on the risk for hyperuricemia was observed. These results suggest that ND2-237 Leu/Met polymorphism modulates the effects of daily alcohol consumption on SUA levels in nonobese Japanese men.

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Purine Catabolism: Links to Mitochondrial Respiration and Antioxidant Defenses?

Cited by 61 publications

References 31 publications

Alterations in tryptophan and purine metabolism in cocaine addiction: a metabolomic study

Alterations in tryptophan and purine metabolism in cocaine addiction: a metabolomic study

Relative contribution of specific sources of systematic errors and analytical imprecision to metabolite analysis by HPLC–ECD

Longevity-associated NADH dehydrogenase subunit-2 237 Leu/Met polymorphism influences the effects of alcohol consumption on serum uric acid levels in nonobese Japanese men

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