dded OH group, has also been found to increase during aging. It is unclear how changes such as these arise, but similar changes seem to be caused be exposure to mutation-causing chemicals, some of which are found in tobacco smoke (Ricklefs and Finch, 1995, 21). Another factor supporting the spontaneous mutations theory may lie in the temporal occurrence of genetic mutations. Certain cancers and abnormal growths seem to appear more frequently as the process of aging continues. Two tumour suppressor genes called p16 and p53 are responsible for slowing cell proliferation, and therefore keep certain cells from becoming cancerous. However, if they become mutated, they do not carry out their function properly so cells with these mutations begin to grow and divide quickly, causing cancer and other growths (Ricklefs and Finch, 1995, 22). Werners syndrome is a disorder that significantly accelerates the aging process starting at around 20 years of age. Molecular geneticist Gerard Schellenburg has suggested that the function of the enzyme helicase, which normally unzips the DNA double helix before replication and removes randomly occurring mutations like base substitutions, does not function properly in people afflicted with Werners. Therefore, the unzipping of the DNA double helix is disrupted and mutations are overlooked (Lafferty et al., 1996, 60). Moreover, DNA occasionally loses one or more bases through the process of spontaneous deletion. This type of mutation seriously affects the mitochondria of the cell, a main source of energy within the cell. Mitochondria have their own DNA, mtDNA, which allows them to self-replicate. The mtDNA encodes for enzymes found within the mitochondria which help produce ATP, energy-storing molecules. During aging, the amount of mtDNA that possess lost segments of DNA increases. Although still unproven, it is believed that this abnormal mtDNA may cause defects in energy production. Most mtDNA deletions occur i...
