Modulation of mitochondrion-mediated oxidative stress by nitric oxide in human placental trophoblastic cells

Nobuhito Goda, Makoto Suematsu, Makio Mukai, Kaoru Kiyokawa, Michiya Natori, Shiro Nozawa, Yuzuru Ishimura

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)


Intracellular hydroperoxide generation in cultured human placental trophoblastic cells (HPTCs) was quantitatively monitored in the presence or absence of an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L- NAME, 1 mM), by digital microfluorography with use of carboxydichlorofluorescein, a hydroperoxide-sensitive fluorogenic probe. In the absence of L-NAME, HPTCs displayed a time-dependent gradual elevation of the fluorescence, suggesting the ability to produce oxidants spontaneously. In the presence of L-NAME, however, the fluorescent response in these cells increased further; the oxidative impact elicited by L-NAME treatment for 30 min was equivalent to that induced by application of 230 μM tert-butyl hydroperoxide for 5 min. This oxidative process was completely blocked by rotenone, a reagent that interferes with electron entry into complex I of the mitochondrial respiratory chain. On the other hand, antimycin A, which blocks mitochondria at the distal site of the ubiquinone pool, potentiated the L- NAME-induced oxidative change. These findings suggest that constitutive levels of nitric oxide production contribute to regulation of mitochondrion- derived intracellular oxidant generation in HPTCs.

Original languageEnglish
Pages (from-to)H1893-H1899
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 40-5
Publication statusPublished - 1996 Nov
Externally publishedYes


  • coenzyme Q
  • iron
  • microcirculation
  • placenta

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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