N-Acetyl cysteine ameliorates hyperglycemia-induced cardiomyocyte toxicity by improving mitochondrial energetics and enhancing endogenous Coenzyme Q9/10 levels

dc.contributor.authorDludla, Phiwayinkosi V.en_ZA
dc.contributor.authorOrlando, Patricken_ZA
dc.contributor.authorSilvestri, Soniaen_ZA
dc.contributor.authorMazibuko-Mbeje, Sithandiwe E.en_ZA
dc.contributor.authorJohnson, Rabiaen_ZA
dc.contributor.authorMarcheggiani, Fabioen_ZA
dc.contributor.authorCirilli, Ileniaen_ZA
dc.contributor.authorMuller, Christo J. F.en_ZA
dc.contributor.authorLouwa, Johanen_ZA
dc.contributor.authorObonye, Nninien_ZA
dc.contributor.authorNyawo, Thembekaen_ZA
dc.contributor.authorNkambule, Bongani B.en_ZA
dc.contributor.authorTiano, Lucaen_ZA
dc.date.accessioned2021-01-28T13:53:19Z
dc.date.available2021-01-28T13:53:19Z
dc.date.issued2019
dc.descriptionCITATION: Dludla, P. V., et al. 2019. N-Acetyl cysteine ameliorates hyperglycemia-induced cardiomyocyte toxicity by improving mitochondrial energetics and enhancing endogenous Coenzyme Q9/10 levels. Toxicology Reports, 6:1240-1245, doi:10.1016/j.toxrep.2019.11.004.
dc.descriptionThe original publication is available at https://www.sciencedirect.com
dc.description.abstractENGLISH ABSTRACT: The diabetic heart has been linked with reduced endogenous levels of coenzyme Q9/10 (CoQ), an important antioxidant and component of the electron transport chain. Although CoQ has displayed cardioprotective potential in experimental models of diabetes, the impact of N-acetyl cysteine (NAC) on mitochondrial energetics and endogenous levels of CoQ remains to be clarified. To explore these effects, high glucose-exposed H9c2 cardiomyocytes were used as an experimental model of hyperglycemia-induced cardiac injury. The results showed that high glucose exposure caused an increased production of reactive oxygen species (ROS), which was associated with impaired mitochondrial energetics as confirmed by a reduction of maximal respiration rate and depleted ATP levels. These detrimental effects were consistent with significantly reduced endogenous CoQ levels and accelerated cell toxicity. Although metformin demonstrated similar effects on mitochondrial energetics and cell viability, NAC demonstrated a more pronounced effect in ameliorating cytosolic and mitochondrial ROS production. Interestingly, the ameliorative effects of NAC against hyperglycemia-induced injury were linked with its capability to enhance endogenous CoQ levels. Although such data are to be confirmed in other models, especially in vivo studies, the overall findings provide additional evidence on the therapeutic mechanisms by which NAC protects against diabetes-induced cardiac injury.en_ZA
dc.description.urihttps://www.sciencedirect.com/science/article/abs/pii/S2214750019304469
dc.description.versionPublisher's version
dc.format.extent6 pagesen_ZA
dc.identifier.citationDludla, P. V., et al. 2019. N-Acetyl cysteine ameliorates hyperglycemia-induced cardiomyocyte toxicity by improving mitochondrial energetics and enhancing endogenous Coenzyme Q9/10 levels. Toxicology Reports, 6:1240-1245, doi:10.1016/j.toxrep.2019.11.004
dc.identifier.issn2214-7500 (online)
dc.identifier.otherdoi:10.1016/j.toxrep.2019.11.004
dc.identifier.urihttp://hdl.handle.net/10019.1/109040
dc.language.isoen_ZAen_ZA
dc.publisherElsevieren_ZA
dc.rights.holderAuthors retain copyrighten_ZA
dc.subjectHyperglycemiaen_ZA
dc.subjectHyperglycemiaen_ZA
dc.subjectL-cysteineen_ZA
dc.subjectUbiquinonesen_ZA
dc.subjectMyocardial diseasesen_ZA
dc.subjectCardiomyocytesen_ZA
dc.subjectDiabetesen_ZA
dc.titleN-Acetyl cysteine ameliorates hyperglycemia-induced cardiomyocyte toxicity by improving mitochondrial energetics and enhancing endogenous Coenzyme Q9/10 levelsen_ZA
dc.typeArticleen_ZA
Files
Original bundle
Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
dludla_cysteine_2019 .pdf
Size:
939.24 KB
Format:
Adobe Portable Document Format
Description:
Download article
License bundle
Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
license.txt
Size:
1.71 KB
Format:
Item-specific license agreed upon to submission
Description: