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We are analyzing https://link.springer.com/article/10.1007/s00228-005-0009-7.

Title:
Antioxidants and endothelial nitric oxide synthesis | European Journal of Clinical Pharmacology
Description:
Oxidative stress in the vasculature has been suggested to contribute to the development of endothelial dysfunction via different mechanisms including LDL oxidation, nitric oxide (NO) scavenging, or oxidation of tetrahydrobiopterin, a critical cofactor of endothelial NO synthase (eNOS). Antioxidants may interfere with these processes and protect NO formed in the endothelium. In particular, ascorbic acid at high concentrations seems to be a prerequisite for sufficient NO bioavailability. Moreover, there is accumulating evidence that ascorbic acid improves tetrahydrobiopterin availability in the vasculature most probably via recycling oxidized tetrahydrobiopterin back to the fully reduced pterin. In addition, ascorbic acid may reduce the α-tocopheroxyl radical and may be required for beneficial vascular effects of α-tocopherol. Recent data have shown that apart from indirect protection of NO from inactivation, α-tocopherol exerts a direct stimulatory effect on eNOS activation via serine 1177 phosphorylation. This effect was amplified by ascorbic acid suggesting that both compounds may act synergistically in optimizing endothelial NO synthesis. The data obtained in cell culture and animal studies are promising, but human long-term studies are needed to determine whether the described mechanisms are active in vivo and may provide a rationale for optimizing dietary or supplementary intake of antioxidant vitamins in certain subsets of patients.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Social Networks

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,642,828 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We don’t know how the website earns money.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

google, scholar, cas, pubmed, article, endothelial, nitric, oxide, tetrahydrobiopterin, synthase, biol, acid, heller, ascorbic, synthesis, dysfunction, vitamin, vascular, chem, werner, clin, res, function, wernerfelmayer, enos, oxidized, role, keaney, med, superoxide, privacy, cookies, content, data, journal, research, antioxidants, mechanisms, oxidation, human, invest, harrison, circ, vita, circulation, implications, european, publish, search, αtocopherol,

Topics {✒️}

oxidized low-density lipoprotein oxidized low-density lipoproteins month download article/chapter endothelial nitric-oxide synthase endothelium-derived nitric oxide targeted transgenic gtp-cyclohydrolase α-tocopherol amplifies phosphorylation l-ascorbic acid endothelial nitric oxide molecular cell biology human long-term studies nitric oxide synthases endothelium-dependent vasodilation article european journal ascorbic acid suggesting full article pdf friedrich-schiller-university intracellular ascorbic acid keaney jf jr privacy choices/manage cookies atherosclerotic heart disease l-arginine availability vascular endothelial dysfunction vascular endothelial function α-tocopherol exerts tocopherol-mediated peroxidation nitric oxide clinical pharmacology aims related subjects beneficial vascular effects human endothelial cells α-tocopheroxyl radical european economic area ca2+/calmodulin-dependent article heller ascorbic acid fully reduced pterin apoe-knockout mice apoe-deficient mice potential antiatherogenic supplement excellent technical assistance tetrahydrobiopterin-dependent preservation inhibiting protein kinase coronary artery disease conditions privacy policy epr-kinetic analysis tetrahydrobiopterin regulatory process potential antiatherogenic mechanisms molecular mechanisms involved long-term vitamin

Questions {❓}

  • Katusic ZS (2001) Vascular endothelial dysfunction: does tetrahydrobiopterin play a role?
  • May JM (2000) How does ascorbic acid prevent endothelial dysfunction?

Schema {🗺️}

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         description:Oxidative stress in the vasculature has been suggested to contribute to the development of endothelial dysfunction via different mechanisms including LDL oxidation, nitric oxide (NO) scavenging, or oxidation of tetrahydrobiopterin, a critical cofactor of endothelial NO synthase (eNOS). Antioxidants may interfere with these processes and protect NO formed in the endothelium. In particular, ascorbic acid at high concentrations seems to be a prerequisite for sufficient NO bioavailability. Moreover, there is accumulating evidence that ascorbic acid improves tetrahydrobiopterin availability in the vasculature most probably via recycling oxidized tetrahydrobiopterin back to the fully reduced pterin. In addition, ascorbic acid may reduce the α-tocopheroxyl radical and may be required for beneficial vascular effects of α-tocopherol. Recent data have shown that apart from indirect protection of NO from inactivation, α-tocopherol exerts a direct stimulatory effect on eNOS activation via serine 1177 phosphorylation. This effect was amplified by ascorbic acid suggesting that both compounds may act synergistically in optimizing endothelial NO synthesis. The data obtained in cell culture and animal studies are promising, but human long-term studies are needed to determine whether the described mechanisms are active in vivo and may provide a rationale for optimizing dietary or supplementary intake of antioxidant vitamins in certain subsets of patients.
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      description:Oxidative stress in the vasculature has been suggested to contribute to the development of endothelial dysfunction via different mechanisms including LDL oxidation, nitric oxide (NO) scavenging, or oxidation of tetrahydrobiopterin, a critical cofactor of endothelial NO synthase (eNOS). Antioxidants may interfere with these processes and protect NO formed in the endothelium. In particular, ascorbic acid at high concentrations seems to be a prerequisite for sufficient NO bioavailability. Moreover, there is accumulating evidence that ascorbic acid improves tetrahydrobiopterin availability in the vasculature most probably via recycling oxidized tetrahydrobiopterin back to the fully reduced pterin. In addition, ascorbic acid may reduce the α-tocopheroxyl radical and may be required for beneficial vascular effects of α-tocopherol. Recent data have shown that apart from indirect protection of NO from inactivation, α-tocopherol exerts a direct stimulatory effect on eNOS activation via serine 1177 phosphorylation. This effect was amplified by ascorbic acid suggesting that both compounds may act synergistically in optimizing endothelial NO synthesis. The data obtained in cell culture and animal studies are promising, but human long-term studies are needed to determine whether the described mechanisms are active in vivo and may provide a rationale for optimizing dietary or supplementary intake of antioxidant vitamins in certain subsets of patients.
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