Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells.

Autor: Ayesha A; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA., Bahnson EM; Department of Cell Biology and Physiology, The University of North Carolina, Chapel Hill, NC 27599, USA., Kayashima Y; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA., Wilder J; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA., Huynh PK; Hackensack Meridian School of Medicine, Nutley, NJ 07110, USA., Hiller S; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA., Maeda-Smithies N; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA., Li F; Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA.
Jazyk: angličtina
Zdroj: Advances in redox research [Adv Redox Res] 2022 Apr; Vol. 4. Date of Electronic Publication: 2022 Jan 11.
DOI: 10.1016/j.arres.2022.100029
Abstrakt: Vitamin B12 (B12) is an essential co-factor for two enzymes in mammalian metabolism and can also act as a mimetic of superoxide dismutase (SOD) converting superoxide (O 2 •‒ ) to hydrogen peroxide (H 2 O 2 ). High oral dose B12 decreases renal O 2 •‒ and post-ischemia/reperfusion injury in mice and protects against damage induced by hypoxia/reperfusion in mouse kidney proximal tubular cells (BU.MPT). O 2 •‒ is unstable and rapidly converted to H 2 O 2 . H 2 O 2 mediates oxidative stress associated with O 2 •‒ . Whether B12 protects against damage induced by H 2 O 2 is unknown. Both BU.MPT cells and mouse brain endothelial cells (bEdn.3) were applied to test the effects of B12 on H 2 O 2 -induced cytotoxicity. Both types of cells were treated with different doses of H 2 O 2 with or without different doses of B12. Cell viability was analyzed 24 h later. H 2 O 2 caused cell death only at a very high dose, and high pharmacological dose of B12 did not prevent this detrimental effect in either cell type. In bEnd.3 cells, transcriptional levels of heme oxygenase-1 (HO-1) increased, while nuclear factor erythroid 2-related factor 2 (Nrf2) decreased by H 2 O 2 . The levels of transcripts were not affected by the B12 treatment. We conclude that the cytotoxic effects of exogenous H 2 O 2 in BU.MPT and bEdn.3 cells are not prevented by B12.
Competing Interests: Declaration of Competing Interest None.
Databáze: MEDLINE
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