Abstract
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.