The Mitochondrial Free Radical Theory of Aging - Supernova: Pliki

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The Mitochondrial Free Radical Theory of Aging
Table 2.1. The human mitochondrial genome, using the standard numbering
conventions, cont.
Position Gene Component of
8527-9207 ATP synthase, subunit 6 Complex V
9207-9990 cytochrome c oxidase, subunit 3 Complex IV
9991-10058 glycine tRNA
10059-10404 NADH dehydrogenase, subunit 3 Complex I
10405-10469 arginine tRNA
10470-10766 NADH dehydrogenase, subunit 4L Complex I
10760-12137 NADH dehydrogenase, subunit 4 Complex I
12138-12206 histidine tRNA
12207-12265 serine tRNA (AGC or AGU)
12266-12336 leucine tRNA (CUN)
12337-14148 NADH dehydrogenase, subunit 5 Complex I
14673-14149 NADH dehydrogenase, subunit 6 Complex I
14674-14742 glutamate tRNA
14747-15887 cytochrome b Complex III
15888-15953 threonine tRNA
15955-16023 proline tRNA
There have also been reports that mitochondrial DNA is more inaccurately replicated
than nuclear DNA, 63 though this has since been disputed. 64 However, in non-dividing cells
(a category which includes nerves and muscle fibres, among others) there is quite definitely
a greater risk of replication error of mtDNA than nuclear DNA, for a much more direct
reason: their nuclear DNA is not being replicated at all, so its risk of replication error is
necessarily zero. Their mitochondrial DNA, on the other hand, is still being replicated (as
will be discussed in the next section), so its risk of replication error, however slight, is greater.
In fact, there is circumstantial evidence that replication error is the main source of mtDNA
mutations in somatic cells. This is that only a small percentage of mtDNA point mutations
seen in vivo, whether in evolution 65 or in cultured cells, 66 are transversions—changes of a
purine to a pyrimidine or vice versa. All the rest are transitions, which change a purine to