**3.4 The zinc material**

The known molecular mechanisms of zinc source are described herein. Zinc differs from the resveratrol, carotenoids and nicotinamide with regard to its mechanism of action in that it influences disease development and immune function by being an essential co-factor in several enzyme functions involving replication, DNA repair and antioxidant defense of cells. Zinc is required for cell replication and DNA polymerase activity (Williams, RO et al 1973). There are two zinc fingers in the DNA binding domain of the poly adenosine diphosphate ribosyl transferase (ADPRT) gene and other DNA repair proteins (Dawat, P. et al 1995; Matsuda, T. et al1 1995; Chiriccolo, M. et al 1993) which contain cysteine residues (i.e. an amino acid), and if these cysteine residues are oxidized at their thiol constituents, they would prevent DNA binding and participation in DNA repair (Mazen et al 1989; de Murcia, G. et al 1989; Pero 1995; Althaus et al 1994). Moreover, superoxide dismutase is an antioxidant enzyme protecting cells from the harmful superoxide anion because this radical is a substrate for the enzymatic reaction that also requires zinc as a cofactor (Brunori and Rotilio 1984).

### **3.5 The DMAE material**

The known molecular mechanisms of DMAE material is described herein. Dimethylaminoethanol (DMAE) material, also known as deanol, is a naturally occurring substance that has been studied as a possible anti-ageing therapy that can also improve cognitive function, reduce neurological stress, improves immunity and DNA repair especially in skin. It is the precursor to choline and may increase acetylcholine levels (Grossman 2005). While choline is known to be the precursor of acetylcholine, a recognized neurotransmitter, DMAE may also prove to offer a more direct approach to this function by moving into the brain, being acted on by an enzyme (methylation), and thereby undergoing conversion into choline directly where it is needed. DMAE inhibits production of the agerelated pigment lipofuscin, which accumulates in all aging tissues. This is significant because cells with increased lipofuscin cause lysosomes to perform poorly, which leads to increased accumulation of poorly functioning mitochondria and increased reactive oxygen species (ROS) production (Terman and Brunk 2006). Evidence also suggests that DMAE decreases the extent of crosslinking of proteins possibly by acting as a free-radical scavenger (Nagy and Nagy 1980).
