Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells
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 (O2 •−) to hydrogen peroxide (H2O2). High oral dose B12 decreases renal O2 •− and post-ischemia/reperfusion injury in mice and protect...
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| Format: | Article |
| Language: | English |
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Elsevier
2022-04-01
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| Series: | Advances in Redox Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2667137922000017 |
| _version_ | 1819003230991941632 |
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| author | Azraa Ayesha Edward M Bahnson Yukako Kayashima Jennifer Wilder Phillip K Huynh Sylvia Hiller Nobuyo Maeda-Smithies Feng Li |
| author_facet | Azraa Ayesha Edward M Bahnson Yukako Kayashima Jennifer Wilder Phillip K Huynh Sylvia Hiller Nobuyo Maeda-Smithies Feng Li |
| author_sort | Azraa Ayesha |
| collection | DOAJ |
| description | 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 (O2 •−) to hydrogen peroxide (H2O2). High oral dose B12 decreases renal O2 •− and post-ischemia/reperfusion injury in mice and protects against damage induced by hypoxia/reperfusion in mouse kidney proximal tubular cells (BU.MPT). O2 •− is unstable and rapidly converted to H2O2. H2O2 mediates oxidative stress associated with O2 •−. Whether B12 protects against damage induced by H2O2 is unknown. Both BU.MPT cells and mouse brain endothelial cells (bEdn.3) were applied to test the effects of B12 on H2O2-induced cytotoxicity. Both types of cells were treated with different doses of H2O2 with or without different doses of B12. Cell viability was analyzed 24 h later. H2O2 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 H2O2. The levels of transcripts were not affected by the B12 treatment. We conclude that the cytotoxic effects of exogenous H2O2 in BU.MPT and bEdn.3 cells are not prevented by B12. |
| first_indexed | 2024-12-20T23:17:42Z |
| format | Article |
| id | doaj.art-7087ec38b4a748338c77583956d8aa4b |
| institution | Directory Open Access Journal |
| issn | 2667-1379 |
| language | English |
| last_indexed | 2024-12-20T23:17:42Z |
| publishDate | 2022-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Advances in Redox Research |
| spelling | doaj.art-7087ec38b4a748338c77583956d8aa4b2022-12-21T19:23:36ZengElsevierAdvances in Redox Research2667-13792022-04-014100029Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cellsAzraa Ayesha0Edward M Bahnson1Yukako Kayashima2Jennifer Wilder3Phillip K Huynh4Sylvia Hiller5Nobuyo Maeda-Smithies6Feng Li7Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USADepartment of Cell Biology and Physiology, The University of North Carolina, Chapel Hill, NC 27599, USADepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USADepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USAHackensack Meridian School of Medicine, Nutley, NJ 07110, USADepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USADepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USADepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 703 Brinkhous-Bullitt Bldg, CB # 7525, Chapel Hill, NC 27599, USA; Corresponding author.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 (O2 •−) to hydrogen peroxide (H2O2). High oral dose B12 decreases renal O2 •− and post-ischemia/reperfusion injury in mice and protects against damage induced by hypoxia/reperfusion in mouse kidney proximal tubular cells (BU.MPT). O2 •− is unstable and rapidly converted to H2O2. H2O2 mediates oxidative stress associated with O2 •−. Whether B12 protects against damage induced by H2O2 is unknown. Both BU.MPT cells and mouse brain endothelial cells (bEdn.3) were applied to test the effects of B12 on H2O2-induced cytotoxicity. Both types of cells were treated with different doses of H2O2 with or without different doses of B12. Cell viability was analyzed 24 h later. H2O2 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 H2O2. The levels of transcripts were not affected by the B12 treatment. We conclude that the cytotoxic effects of exogenous H2O2 in BU.MPT and bEdn.3 cells are not prevented by B12.http://www.sciencedirect.com/science/article/pii/S2667137922000017Vitamin B12Hydrogen peroxideBU.MPT cellsbEdn.3 cellsCell viability |
| spellingShingle | Azraa Ayesha Edward M Bahnson Yukako Kayashima Jennifer Wilder Phillip K Huynh Sylvia Hiller Nobuyo Maeda-Smithies Feng Li Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells Advances in Redox Research Vitamin B12 Hydrogen peroxide BU.MPT cells bEdn.3 cells Cell viability |
| title | Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells |
| title_full | Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells |
| title_fullStr | Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells |
| title_full_unstemmed | Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells |
| title_short | Vitamin B12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells |
| title_sort | vitamin b12 does not increase cell viability after hydrogen peroxide induced damage in mouse kidney proximal tubular cells and brain endothelial cells |
| topic | Vitamin B12 Hydrogen peroxide BU.MPT cells bEdn.3 cells Cell viability |
| url | http://www.sciencedirect.com/science/article/pii/S2667137922000017 |
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