Bioscience Biotechnology and Biochemistry · 2000 · 34 citations · 13 references
Life SciencesCell BiologyPharmacologyApoptosisCellular BiochemistryCellular MetabolismApoptosis PharmacologyCell DeathDna DamageNicotinamide Adenine Dinucleotide MetabolismNucleotide MetabolismConcentrationNickel-induced ApoptosisNicotinamide Adenine Dinucleotide (Nad+) Metabolism
In our previous paper, we have reported that niacin-related compounds, particularly picolinic acid, dipicolinic acid, and isonicotinamide, induced apoptosis in HL-60 cells but that niacin did not. Moreover, picolinamide, N1-methylnicotinamide, 6-aminonicotinamide, quinolinic acid, and cinchomeronic acid also had the function of DNA fragmentation in HL-60 cells analyzed by flow cytometry, the ratio of DNA fragmentation finally being about 40% after treatment with these compounds at 10 mM for 24 h. In this study, we found that these compounds also induced apoptosis in HL-60 cells. The wide-spectrum caspase inhibitors prevented DNA fragmentation induced by these compounds. Interestingly, 6-aminonicotinamide induced apoptosis at a comparatively low concentration, while picolinic acid, dipicolinic acid, and isonicotinamide did not at 1 mM. Our results suggest that both NAD metabolism and NAD biosynthesis may be related to the process of apoptosis induced by niacin-related compounds.
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Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c
Xuesong Liu, Caryn Naekyung Kim, Jie Yang et al. · Cell · 1996 · 5.2K citations · Full text
Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE
Yuri Lazebnik, Scott H. Kaufmann, Serge Desnoyers et al. · Nature · 1994 · 2.6K citations