Endothelial nitric oxide synthase is up-regulated in the umbilical cord in pregnancies complicated with intrauterine growth retardation

In Vivo. 2009 Sep-Oct;23(5):727-32.

Abstract

Background: NO and NO synthases (NOS) play an important role in the physiology of the fetomaternal blood circulation, although their expression in pathological conditions is unclear. Intrauterine growth retardation (IUGR) is a disorder most probably caused by abnormality of the fetomaternal bloodflow.

Materials and methods: The expression of endothelial NOS (ecNOS) from arteria umbilicalis and the nitrite and peroxynitrite level of umbilical blood were determined. Major consequences of peroxynitrite toxicity are lipid peroxidation and glutathione depletion; these parameters were also measured. Finally, superoxide dismutase (SOD) activity was assayed to evaluate the level of superoxide anions.

Results: Elevated expression of ecNOS was found to be coupled with significantly lower SOD activity and glutathione level, and increased lipid peroxidation in IUGR neonates.

Conclusion: The increased NO indices could represent a compensatory effort to improve placental bloodflow, but in IUGR neonates it is coupled with inadequate antioxidant defence, resulting in significant oxidative stress.

MeSH terms

  • Adult
  • Endothelium, Vascular / enzymology*
  • Erythrocyte Deformability
  • Female
  • Fetal Blood / chemistry
  • Fetal Growth Retardation / blood
  • Fetal Growth Retardation / enzymology*
  • Gene Expression
  • Glutathione / analysis
  • Humans
  • Infant, Newborn
  • Lipid Peroxidation
  • Male
  • Nitric Oxide Synthase Type III / genetics*
  • Nitric Oxide Synthase Type III / metabolism
  • Nitrites / blood
  • Oxidative Stress
  • Peroxynitrous Acid / blood
  • Pregnancy
  • RNA, Messenger / metabolism
  • Superoxide Dismutase
  • Umbilical Arteries / enzymology*
  • Up-Regulation

Substances

  • Nitrites
  • RNA, Messenger
  • Peroxynitrous Acid
  • Nitric Oxide Synthase Type III
  • Superoxide Dismutase
  • Glutathione