Nicotinamide, a missing link in the early stress response in eukaryotic cells: a hypothesis with special reference to oxidative stress in plants.
A hypothesis is presented suggesting that nicotinamide (NIC) is an initial signal substance in the response of eukaryotic cells to conditions which cause DNA-strand breakage, especially in connection with oxidative stress. In the stressed cell, NIC is released as a result of the activity of poly(ADP-ribose)polymerase (PADPRP). PADPRP is known to be activated by DNA-strand breakage, caused by e.g. oxidative stress or mutagens. NIC and its metabolite trigonelline (N-methylnicotinic acid) can induce defensive metabolism at the gene level. Connections between NIC and DNA-methylation are also considered. This hypothesis is discussed in the light of own observations and literature reports.
Berglund
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Department of Biochemistry and Biotechnology, Royal Institute of Technology, Stockholm, Sweden.
D000220:Adaptation, Biological; D000470:Alkaloids / Q000378:metabolism; D004249:DNA Damage; D005057:Eukaryotic Cells / Q000378:metabolism; D008954:Models, Biological; D009536:Niacinamide / Q000378:metabolism*; D010084:Oxidation-Reduction; D010944:Plants / Q000378:metabolism*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D015398:Signal Transduction
D000470:Alkaloids; D009536:Niacinamide; C009560:trigonelline; D011065:Poly(ADP-ribose) Polymerases