Niacin may reduce apoptosis, preclinical study shows
Highlights
- Nicotinic acid & niacinamide exert anti-apoptotic action
- Action appears to be multifactorial, including DNA repair
- Action appears unrelated to reducing oxidative stress
Summary
The aim of this in-vitro study was to evaluate the effect of the NAD+ precursors nicotinic acid (NA) and niacinamide (NAM) on cell death (apoptosis).
To induce apoptosis, the researchers pre-treated Jurkat cells (derived from a T-cell lymphoma) with the bile salt sodium deoxycholate (NaDOC). At high physiologic levels, NaDOC is known to activate many stress-response pathways (e.g., DNA damage, oxidative stress, endoplasmic reticulum stress, protein misfolding) and induce apoptosis in various cell types.
Results indicate that both NA and NAM were found to protect the cells against NaDOC-induced apoptosis.
The mechanism of action appears unrelated to reducing oxidative stress. Rather, as NAD+ precursors, NA and NAM may be involved in increasing cell viability via multiple mechanisms directed at various stressors and probably aid in DNA repair. The DNA repair activity is attributed, in part, to the role of NAD+ as a substrate for poly(ADP-ribose)polymerase (PARP) as well as the ability to induce glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Both PARP and GAPDH are key enzymes involved in DNA repair.
While more research is needed, the authors note that these preliminary findings suggest that NAD+ precursors such as NA and NAM may offer anti-aging benefits as well as therapeutic value for diseases associated with increased apoptosis and DNA damage, including cancer, inflammatory disease, neurodegenerative disease, among others.
Reference
Crowley CL, Payne CM, Bernstein H, Bernstein C, Roe D. The NAD+ precursors, nicotinic acid and nicotinamide protect cells against apoptosis induced by a multiple stress inducer, deoxycholate. Cell Death Differ. 2000;7(3):314-326. PMID: 10745276.
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