Evidence map›Paper›PMID 25379360›Full record

ArticleIEEE journal of translational engineering in health and medicine2013

Novel Flurometric Tool to Assess Mitochondrial Redox State of Isolated Perfused Rat Lungs after Exposure to Hyperoxia.

R Sepehr, S H Audi, K S Staniszewski, S T Haworth, E R Jacobs, M Ranji

Abstract read
In one paragraph

Article in IEEE journal of translational engineering in health and medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. In vivo molecular imaging stratifies rats with different susceptibilities to hyperoxic acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022
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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

6 authors.

R Sepehr
S H Audi
K S Staniszewski
S T Haworth
E R Jacobs
M Ranji

Funding

Clincal and Translational Science AwardUL1TR000055 · NCATS · MEDICAL COLLEGE OF WISCONSIN · PI SHAKER, REZA NONE · 2012 to 2015
$11.3M
PULMONARY ARTERY ENDOTHELIAL CELLS AND SHEAR STRESSR01HL049294 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI JACOBS, ELIZABETH R · 1994 to 2010
$3.1M
Novel Diagnostics to Detect Lung InjuryI01BX001681 · VA · CLEMENT J. ZABLOCKI VA MEDICAL CENTER · PI JACOBS, ELIZABETH R · 2013 to 2016
–
BLRD VA I01 BX001681NCATS NIH HHS UL1 TR000055NHLBI NIH HHS R01 HL049294
6 · The paper itself

Abstract

Recently we demonstrated the utility of optical fluorometry to detect a change in the redox status of mitochondrial autofluorescent coenzymes NADH (Nicotinamide Adenine Dinucleotide) and FAD (oxidized form of Flavin Adenine Dinucleotide (FADH2,)) as a measure of mitochondrial function in isolated perfused rat lungs (IPL). The objective of this study was to utilize optical fluorometry to evaluate the effect of rat exposure to hyperoxia (>95% O2 for 48 hours) on lung tissue mitochondrial redox status of NADH and FAD in a nondestructive manner in IPL. Surface NADH and FAD signals were measured before and after lung perfusion with perfusate containing rotenone (ROT, complex I inhibitor), potassium cyanide (KCN, complex IV inhibitor), and/or pentachlorophenol (PCP, uncoupler). ROT- or KCN-induced increase in NADH signal is considered a measure of complex I activity, and KCN-induced decrease in FAD signal is considered a measure of complex II activity. The results show that hyperoxia decreased complex I and II activities by 63% and 55%, respectively, as compared to lungs of rats exposed to room air (normoxic rats). Mitochondrial complex I and II activities in lung homogenates were also lower (77% and 63%, respectively) for hyperoxic than for normoxic lungs. These results suggest that the mitochondrial matrix is more reduced in hyperoxic lungs than in normoxic lungs, and demonstrate the ability of optical fluorometry to detect a change in mitochondrial redox state of hyperoxic lungs prior to histological changes characteristic of hyperoxia.

Indexed as

Flavin Adenine Dinucleotide (FADH2)lung surface fluorometrymitochondrial redoxNADH dehydrogenase (complex I)Nicotinamide Adenine Dinucleotide (NADH)succinate dehydrogenase (complex II)

Identifiers

PMID25379360
PMCPMC4219590

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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.