Apoptosis induced by nicotinamide-related compounds and quinolinic acid in HL-60 cells.
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.
Ogata
S
S
Laboratory of Biological Chemistry, Faculty of Bioresources, Mie University, Tsu, Japan.
Takeuchi
M
M
Fujita
H
H
Shibata
K
K
Okumura
K
K
Taguchi
H
H
D017209:Apoptosis / Q000187:drug effects*; D004587:Electrophoresis, Agar Gel; D005434:Flow Cytometry; D018922:HL-60 Cells; D006801:Humans; D009536:Niacinamide / Q000031:analogs & derivatives / Q000494:pharmacology*; D017378:Quinolinic Acid / Q000494:pharmacology*
D009536:Niacinamide; D017378:Quinolinic Acid