Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism

Table 3 NF-κB, p53, c-Jun and caspase-3 molecules are involved in vitamin K3 (VK3)- and vitamin C (VC)-induced apoptosis in Jurkat cells.

Jurkat cells (1 × 10⁶ cell/mL) were left untreated or treated with specific NF-κB, p53, c-Jun and caspase-3 inhibitors such as ammonium pyrrolidinedithiocarbamate (PDTC, 10 nM), pifithrin-α (PFT, 50 nM), SP600125 (1 μM) and NSCI (10 μM) alone or in presence of VK3 (10 μM), VC (10 mM), VC (10 mM): VK3 (10 μM) at 37 °C for 24 h. After this time, nuclear morphologic and mitochondrial membrane potential changes as a result of NF-κB, p53, c-Jun, and caspase-3 activation were evaluated using acridine orange/ethidium bromide (AO/EB) and DiOC₆(3) staining, as described in Materials and Methods. High polarized and low-polarized mitochondria (green fluorescent DiOC₆(3) high/low positive cells) and positive apoptotic nuclei percentage is expressed as mean of percentage (%) ± S.D. from three independent experiments. A one-way ANOVA analysis was performed, p < 0.0001. ^aSignificantly different from VK3 by Bonferroni post-ho c analysis for DiOC₆(3) and AO/EB. ^bSignificantly different from VC by Bonferroni post-ho c analysis for DiOC₆(3) and AO/EB. ^cSignificantly different from VK3-VC by Bonferroni post-ho c analysis for DiOC₆(3) and AO/EB.

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