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 (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.