Analysis of reduced forms of biopterin in biological tissues and fluids

Fukushima, Takeshi; Nixon, J. C.

doi:10.1016/0003-2697(80)90336-x

Cited by 706 publications

(365 citation statements)

References 34 publications

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“…1~ standard). As expected, a comparison of HPLC chromatograms with the reference pterins showed that fraction 'bl' from brain tissue [17] and from the mast cells was identical with 6-biopterin. Fraction 'b2' which was only found in mast cells was identical with 7-biopterin.…”

Section: Resultssupporting

confidence: 78%

“…Its retention time was clearly different from the other pterins in at least one of the solvent systems I, II, or IIl. Alkaline iodine o~idation of the cell extract destroys H~biopterin, but oxidizes H,.biopterin to biopterin [17]. After this treatment neither 6-nor 7-biopterin was detectable in the extracts of both mast cells and brain tissue.…”

Section: Resultsmentioning

confidence: 95%

“…H,~biopterin was oxidized by acidic iodine, deproteinized and pre.purlfied by cationexchange as previously described [15], Modifications of the method have been detailed in [16]. For the quantification of dihydrobiopterin atiqaots of the acidic extracts were brought to pH 13, Oxidation with iodine (in 0.1 M NaOH) was followed by addition of 2 N HCI to change biopterin back in:o its cationic form [17]. The pre.eolumn and the separation column (250 × 4,6 ram) of the HPLC system consisted of Shandon Hypersil.ODS 5 jam, A Shlmadzu model RF 535 HPLC fluorescence detector was interfaced with a Shlmadzu C-R6A Chromatopae analytical data system.…”

Section: Andermine Analysismentioning

confidence: 99%

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Tetrahydro‐6‐biopterin is associated with tetrahydro‐7‐biopterin in primary murine mast cells

Ziegler

Hültner²

1992

FEBS Letters

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Marine bone marrow-deriv~ mast cells proliferate in response to interleukin 3. In addition to 6.biopterin, 7-biopterin was identified in th~¢ ~lls by HPLC analysis of iodine ~!a.~ed e.,,.:racts and by alkaline pen~anganate oxidation to the 6-and 7,carbox~lic acids. 7-Biopterin comprised 31.9 (_+ 7.7)% of the total biopterin. It was absent in cells which were grown with of t.-p-chlorophenylalani~e, an inhibitor of try. ptophan 5-monoosygenase. Both 6-and 7.biopterin were present in the cell as their tetrahydro forms. From these dala we conclude that 7-biopterin, in contrast to e.g. brain tissue, regularly occurs as a normal metabolite in primary mast cells and that it is generated during hydroxylation of tryptophan.

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Section: Resultssupporting

confidence: 78%

Section: Resultsmentioning

confidence: 95%

Section: Andermine Analysismentioning

confidence: 99%

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Tetrahydro‐6‐biopterin is associated with tetrahydro‐7‐biopterin in primary murine mast cells

Ziegler

Hültner²

1992

FEBS Letters

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“…Thus, heterologous PAH expression in skeletal and cardiac muscle alone without BH 4 skeletal muscle in only small amounts (0.08 g/g wet weight versus 1.6 g/g wet weight in the liver). 16 Total biopterin was measured in liver and skeletal muscle homogenate from C57Bl/6J mice in our colony by Dr Sheldon Milstien, Bethesda, MD, USA. Murine liver contained 3.0 ± 0.9 pmol biopterin per milligram liver wet weight (mean ± s.d.…”

Section: Effect Of Muscle Pah Expression Upon Hyperphenylalaninemic Micementioning

confidence: 99%

Metabolic engineering as therapy for inborn errors of metabolism – development of mice with phenylalanine hydroxylase expression in muscle

Harding¹,

Wild²,

Chang³

et al. 1998

Gene Ther

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Treatment of many inherited liver enzyme deficiencies muscle. These mice exhibited hyperphenylalaninemia at requires the removal of toxic intermediate metabolites frombaseline, but serum phenylalanine levels decreased sigthe blood of affected individuals. We propose that circulatnificantly when the mice were supplemented with tetrahyding toxins can be adequately cleared and disease phenorobiopterin (BH 4 ), a required cofactor for PAH. This is the type influenced by enzyme expressed in tissues other than first demonstration that a liver-specific enzyme, when the liver. Phenylalanine hydroxylase (PAH) activity was expressed in a heterologous tissue and supplied with constitutively expressed in skeletal and cardiac muscle of necessary cofactors, can effectively clear toxic metabolites transgenic mice which carried the PAH cDNA under the from the circulation of individuals with inherited enzyme transcriptional control of the mouse muscle creatine kinase deficiency. This result suggests that gene therapy targeted promoter. Muscle PAH-expressing mice were bred to liver to heterologous tissues, such as muscle, will be effective PAH-deficient, hyperphenylalaninemic mice to yield proin the treatment of selected inborn errors of metabolism. geny that lack PAH activity in liver but express PAH in

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“…Protein carbonylation (PC) assays were based on the photometric method of Levine et al 24 . Plasma tetrahydrobiopterin (BH 4 ) level was measured using high performance liquid chromatography based on the method of Fukushima and Nixon 25 4 to biopterin and the alkaline-stable oxidized biopterin level (BH 2 plus biopterin) obtained using alkaline iodine, which oxidizes only BH 2 to biopterin. These methods were described in a more detailed way earlier 27 .…”

Section: Measurement Of Oxidative Stress Parametersmentioning

confidence: 99%

Genetic predisposition in patients with hypertension and normal ejection fraction to oxidative stress

Fazakas

Szelényi

Szénási

et al. 2016

Journal of the American Society of Hypertension

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The role of oxidative stress (OXS) due to myocardial nitric oxide synthase (NOS) uncoupling related to oxidative depletion of its cofactor tetrahydrobiopterin (BH 4 ) emerged in the pathogenesis of heart failure with preserved ejection fraction (HFPEF).We determined the prevalence of 6 single nucleotide polymorphisms (SNPs) of genes encoding enzymes related to OXS, BH 4 metabolism and NOS function in >60-year-old 94 patients with hypertension and 18 age-matched controls with normal EF. Using echocardiography 56/94(60%) patients with hypertension had left ventricular (LV) diastolic dysfunction (HTDD+ group), 38/94(40%) patients had normal LV diastolic function (HTDDgroup). Four SNPs (rs841, rs3783641, rs10483639, rs807267) of guanosine triphosphate cyclohydrolase-1, the rate limiting enzyme in BH 4 synthesis, 1 (rs4880) of manganese superoxide dismutase, and 1 (rs1799983) of endothelial NOS genes were genotyped using real time PCR method and Taqman probes. Protein carbonylation (PC), BH 4 and total biopterin levels were measured from plasma samples. No between-groups difference in minor allele frequency (MAF) of SNPs was found. We calculated a genetic score indicating risk for OXS based on the MAFs of the SNPs. A high genetic risk for OXS was significantly associated with HTDD+ even after adjustment for confounding variables [OR(95%CI):4.79(1.12-20.54); p=0.035]. In both patient groups PC (p<0.05 for both), plasma BH 4 (p<0.01 for both) and in the HTDD+ group total biopterin (p<0.05) increased vs. controls. In conclusion, in patients with hypertension and normal EF, a potential precursor of HFPEF, a partly genetically determined increased OXS seems to be associated with the presence of LV diastolic dysfunction.key words: hypertension, heart failure with preserved ejection fraction, oxidative stress 3

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Analysis of reduced forms of biopterin in biological tissues and fluids

Cited by 706 publications

References 34 publications

Tetrahydro‐6‐biopterin is associated with tetrahydro‐7‐biopterin in primary murine mast cells

Tetrahydro‐6‐biopterin is associated with tetrahydro‐7‐biopterin in primary murine mast cells

Metabolic engineering as therapy for inborn errors of metabolism – development of mice with phenylalanine hydroxylase expression in muscle

Genetic predisposition in patients with hypertension and normal ejection fraction to oxidative stress

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