Evidence map›Paper›PMID 9620869›Full record

ArticleThe Biochemical journal1998

Functional implications of nitric oxide produced by mitochondria in mitochondrial metabolism.

C Giulivi

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
11.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 214 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. The Role of Nitric Oxide in Cancer: Master Regulator or NOt?International journal of molecular sciences · 2020
    Review
  6. Article
  7. The Role of Antioxidant Enzymes in the Ovaries.Oxidative medicine and cellular longevity · 2017
    Review
  8. NO-sGC Pathway Modulates CaFrontiers in physiology · 2017
    Article
  9. Select nutrients and their effects on conceptus development in mammals.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2015
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Measuring mitochondrial function in intact cardiac myocytes.Journal of molecular and cellular cardiology · 2012
    Review
  18. Review
  19. Article
  20. Nitration of specific tyrosines in FoF1 ATP synthase and activity loss in aging.American journal of physiology. Endocrinology and metabolism · 2010
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

C GiuliviDepartment of Molecular Pharmacology and Toxicology, University of Southern California, 1985 Zonal Ave., Los Angeles, CA 90033, USA. cgiulivi@hsc.edu
University of Southern California · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
NIDDK NIH HHS P30 DK48522
6 · The paper itself

Abstract

The effects of endogenous production of NO., catalysed by the mitochondrial nitric oxide synthase (NOS), on mitochondrial metabolism were studied. The respiratory rates of intact mitochondria in State 4 were decreased by 40% and 28% with succinate and malate-glutamate, respectively, in the presence of L-arginine (L-Arg); conversely, the O2 uptake with NG-methyl-L-arginine (NMMA), a competitive inhibitor of NOS, was increased. The production of NO. and the inhibition of the respiratory rates were dependent on the metabolic state in which mitochondria were maintained: NO. production was probably supported by mitochondrial NADPH, the latter maintained by the energy-dependent transhydrogenase. In addition to the decline in the respiratory rate, an inhibition of ATP synthesis was also observed (40-50%) following supplementation with L-Arg. The dependence of the respiratory rates of mitochondria in State 3 and cytochrome oxidase activities on O2 concentrations with either L-Arg or NMMA indicated that both processes were competitively inhibited by NO. at the cytochrome oxidase level. This inhibition can be explained by the interaction of NO. with cytochrome oxidase at the binuclear centre. The role of NO. as a physiological modulator of cytochrome oxidase is discussed in terms of cellular metabolism.

Indexed as

Adenosine TriphosphateAnimalsCell RespirationElectron Transport Complex IVFree RadicalsGasesIn Vitro TechniquesMitochondria, LiverNitratesNitric OxideOxidation-ReductionOxygen ConsumptionPhosphorylationRatsAdenosine TriphosphateElectron Transport Complex IVFree RadicalsGasesNitratesNitric Oxideperoxynitric acid

Identifiers

PMID9620869
PMCPMC1219527
OpenAlexW2395675726

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.