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Verfasst von:Zhang, Shiqi [VerfasserIn]   i
 Ntasis, Emmanouil [VerfasserIn]   i
 Krämer, Bernhard [VerfasserIn]   i
 Yard, Benito A. [VerfasserIn]   i
 Hauske, Sibylle J. [VerfasserIn]   i
Titel:Hyperglycemia does not affect iron mediated toxicity of cultured endothelial and renal tubular epithelial cells
Titelzusatz:influence of L-carnosine
Verf.angabe:Shiqi Zhang, Emmanouil Ntasis, Sarah Kabtni, Jaap van den Born, Gerjan Navis, Stephan J. L. Bakker, Bernhard K. Krämer, Benito A. Yard, and Sibylle J. Hauske
Jahr:2016
Umfang:9 S.
Fussnoten:Gesehen am 26.02.2019
Titel Quelle:Enthalten in: Journal of diabetes research
Ort Quelle:New York, NY [u.a.] : Hindawi, 2013
Jahr Quelle:2016
Band/Heft Quelle:2016(2016) Artikel-Nummer 8710432, 9 Seiten
ISSN Quelle:2314-6753
Abstract:Iron has been suggested to affect the clinical course of type 2 diabetes (T2DM) as accompanying increased intracellular iron accumulation may provide an alternative source for reactive oxygen species (ROS). Although carnosine has proven its therapeutic efficacy in rodent models of T2DM, little is known about its efficacy to protect cells from iron toxicity. We sought to assess if high glucose (HG) exposure makes cultured human umbilical vein endothelial cells (HUVECs) and renal proximal tubular epithelial cells (PTECs) more susceptible to metal induced toxicity and if this is ameliorated by L-carnosine. HUVECs and PTECs, cultured under normal glucose (5 mM, NG) or HG (30 mM), were challenged for 24 h with FeCl3. Cell viability was not impaired under HG conditions nor did HG increase susceptibility to FeCl3. HG did not change the expression of divalent metal transporter 1 (DMT1), ferroportin (IREG), and transferrin receptor protein 1 (TFRC). Irrespective of glucose concentrations L-carnosine prevented toxicity in a dose-dependent manner, only if it was present during the FeCl3 challenge. Hence our study indicates that iron induced cytotoxicity is not enhanced under HG conditions. L-Carnosine displayed a strong protective effect, most likely by chelation of iron mediated toxicity.
DOI:doi:10.1155/2016/8710432
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: http://dx.doi.org/10.1155/2016/8710432
 Volltext: https://www.hindawi.com/journals/jdr/2016/8710432/
 DOI: https://doi.org/10.1155/2016/8710432
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:158813248X
Verknüpfungen:→ Zeitschrift

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