ArticleBiochemistry2013
Effect of nitric oxide on naphthoquinone toxicity in endothelial cells: role of bioenergetic dysfunction and poly (ADP-ribose) polymerase activation.
Article in Biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Vitamin E Attenuates Red-Light-Mediated Vasodilation: The Benefits of a Mild Oxidative Stress.Antioxidants (Basel, Switzerland) · 2024Article
- The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage.Frontiers in endocrinology · 2021Review
- Inhibition of oxidative metabolism by nitric oxide restricts EMCV replication selectively in pancreatic beta-cells.The Journal of biological chemistry · 2020Article
- Nitric Oxide Circumvents Virus-Mediated Metabolic Regulation during Human Cytomegalovirus Infection.mBio · 2020Article
- Inhibition of mitochondrial oxidative metabolism attenuates EMCV replication and protects β-cells from virally mediated lysis.The Journal of biological chemistry · 2020Article
- Peroxiredoxin 1 plays a primary role in protecting pancreatic β-cells from hydrogen peroxide and peroxynitrite.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- The Role of Metabolic Flexibility in the Regulation of the DNA Damage Response by Nitric Oxide.Molecular and cellular biology · 2019Article
- Pancreatic β-cells detoxify HThe Journal of biological chemistry · 2019Article
- Dual Role of Nitric Oxide in Regulating the Response of β Cells to DNA Damage.Antioxidants & redox signaling · 2018Review
- Cardiomyocyte Differentiation Promotes Cell Survival During Nicotinamide Phosphoribosyltransferase Inhibition Through Increased Maintenance of Cellular Energy Stores.Stem cells translational medicine · 2017Article
- Aloe vera toxic effects: expression of inducible nitric oxide synthase (iNOS) in testis of Wistar rat.Iranian journal of basic medical sciences · 2015Article
- ATM facilitates mouse gammaherpesvirus reactivation from myeloid cells during chronic infection.Virology · 2015Article
- Inhibition of an NAD⁺ salvage pathway provides efficient and selective toxicity to human pluripotent stem cells.Stem cells translational medicine · 2015Article
- How the location of superoxide generation influences the β-cell response to nitric oxide.The Journal of biological chemistry · 2015Article
- Cancer cell metabolism and the modulating effects of nitric oxide.Free radical biology & medicine · 2015Review
- L-carnosine alters some hemorheologic and lipid peroxidation parameters in nephrectomized rats.Medical science monitor : international medical journal of experimental and clinical research · 2014Article
- Do β-cells generate peroxynitrite in response to cytokine treatment?The Journal of biological chemistry · 2013Article
- Regulation of ATR-dependent DNA damage response by nitric oxide.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
When produced at physiological levels, reactive oxygen species (ROS) can act as signaling molecules to regulate normal vascular function. Produced under pathological conditions, ROS can contribute to the oxidative damage of cellular components (e.g., DNA and proteins) and trigger cell death. Moreover, the reaction of superoxide with nitric oxide (NO) produces the strong oxidant peroxynitrite and decreases NO bioavailability, both of which may contribute to activation of cell death pathways. The effects of ROS generated from the 1,4-naphthoquinones alone and in combination with NO on the activation status of poly(ADP-ribose) polymerase (PARP) and cell viability were examined. Treatment with redox cycling quinones activates PARP, and this stimulatory effect is attenuated in the presence of NO. Mitochondria play a central role in cell death signaling pathways and are a target of oxidants. We show that simultaneous exposure of endothelial cells to NO and ROS results in mitochondrial dysfunction, ATP and NAD(+) depletion, and cell death. Alone, NO and ROS have only minor effects on cellular bioenergetics. Further, PARP inhibition does not attenuate reduced cell viability or mitochondrial dysfunction. These results show that concomitant exposure to NO and ROS impairs energy metabolism and triggers PARP-independent cell death. While superoxide-mediated PARP activation is attenuated in the presence of NO, PARP inhibition does not modify the loss of mitochondrial function or adenine and pyridine nucleotide pools and subsequent bioenergetic dysfunction. These findings suggest that the mechanisms by which ROS and NO induce endothelial cell death are closely linked to the maintenance of mitochondrial function and not overactivation of PARP.
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Registered trials
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.