Selective Inhibition of the 12-Lipoxygenase Pathway of Arachidonic Acid Metabolism by L-Arginine or Sodium Nitroprusside in Intact Human Platelets

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Abstract

L-arginine (1-100 μM) or sodium nitroprusside (1-100 μM) caused a concentration dependent decrease in the metabolism of exogenously added arachidonic acid via the 12-lipoxygenase pathway in intact human platelets, as determined by the use of an HPLC assay. NG-monomethyl-L-arginine, but not the D-isomer of this compound, diminished the inhibitory effect of L-arginine. The D isomer of arginine had no effect. The cyclooxygenase pathway was much less susceptible to these effects. This study indicated that nitric oxide formed in intact human platelets selectively inhibited 12-lipoxygenase over that of cyclooxygenase and suggests that such inhibition may be an important regulatory mechanism.

Original languageEnglish
Pages (from-to)1630-1634
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume200
Issue number3
DOIs
Publication statusPublished - May 15 1994
Externally publishedYes

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Arachidonate 12-Lipoxygenase
Nitroprusside
Platelets
Arachidonic Acid
Metabolism
Arginine
Blood Platelets
Prostaglandin-Endoperoxide Synthases
Isomers
omega-N-Methylarginine
Assays
Nitric Oxide
High Pressure Liquid Chromatography

ASJC Scopus subject areas

  • Molecular Biology
  • Biophysics
  • Biochemistry

Cite this

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title = "Selective Inhibition of the 12-Lipoxygenase Pathway of Arachidonic Acid Metabolism by L-Arginine or Sodium Nitroprusside in Intact Human Platelets",
abstract = "L-arginine (1-100 μM) or sodium nitroprusside (1-100 μM) caused a concentration dependent decrease in the metabolism of exogenously added arachidonic acid via the 12-lipoxygenase pathway in intact human platelets, as determined by the use of an HPLC assay. NG-monomethyl-L-arginine, but not the D-isomer of this compound, diminished the inhibitory effect of L-arginine. The D isomer of arginine had no effect. The cyclooxygenase pathway was much less susceptible to these effects. This study indicated that nitric oxide formed in intact human platelets selectively inhibited 12-lipoxygenase over that of cyclooxygenase and suggests that such inhibition may be an important regulatory mechanism.",
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T1 - Selective Inhibition of the 12-Lipoxygenase Pathway of Arachidonic Acid Metabolism by L-Arginine or Sodium Nitroprusside in Intact Human Platelets

AU - Nakatsuka, Mikiya

AU - Osawa, Y.

PY - 1994/5/15

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N2 - L-arginine (1-100 μM) or sodium nitroprusside (1-100 μM) caused a concentration dependent decrease in the metabolism of exogenously added arachidonic acid via the 12-lipoxygenase pathway in intact human platelets, as determined by the use of an HPLC assay. NG-monomethyl-L-arginine, but not the D-isomer of this compound, diminished the inhibitory effect of L-arginine. The D isomer of arginine had no effect. The cyclooxygenase pathway was much less susceptible to these effects. This study indicated that nitric oxide formed in intact human platelets selectively inhibited 12-lipoxygenase over that of cyclooxygenase and suggests that such inhibition may be an important regulatory mechanism.

AB - L-arginine (1-100 μM) or sodium nitroprusside (1-100 μM) caused a concentration dependent decrease in the metabolism of exogenously added arachidonic acid via the 12-lipoxygenase pathway in intact human platelets, as determined by the use of an HPLC assay. NG-monomethyl-L-arginine, but not the D-isomer of this compound, diminished the inhibitory effect of L-arginine. The D isomer of arginine had no effect. The cyclooxygenase pathway was much less susceptible to these effects. This study indicated that nitric oxide formed in intact human platelets selectively inhibited 12-lipoxygenase over that of cyclooxygenase and suggests that such inhibition may be an important regulatory mechanism.

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