Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Maximum life span
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
==Correlation with DNA repair capacity== {{Main|DNA damage theory of aging}} Accumulated DNA damage appears to be a limiting factor in the determination of maximum life span. The theory that DNA damage is the primary cause of aging, and thus a principal determinant of maximum life span, has attracted increased interest in recent years. This is based, in part, on evidence in humans and mice that inherited deficiencies in DNA repair genes often cause accelerated aging.<ref>{{cite journal | vauthors = Hoeijmakers JH | title = DNA damage, aging, and cancer | journal = The New England Journal of Medicine | volume = 361 | issue = 15 | pages = 1475–85 | date = October 2009 | pmid = 19812404 | doi = 10.1056/NEJMra0804615 }}</ref><ref name=Diderich>{{cite journal | vauthors = Diderich K, Alanazi M, Hoeijmakers JH | title = Premature aging and cancer in nucleotide excision repair-disorders | journal = DNA Repair | volume = 10 | issue = 7 | pages = 772–80 | date = July 2011 | pmid = 21680258 | doi = 10.1016/j.dnarep.2011.04.025 | pmc = 4128095 }}</ref><ref name="Freitas_2011">{{cite journal | vauthors = Freitas AA, de Magalhães JP | title = A review and appraisal of the DNA damage theory of ageing | journal = Mutation Research | volume = 728 | issue = 1–2 | pages = 12–22 | date = 2011 | pmid = 21600302 | doi = 10.1016/j.mrrev.2011.05.001 }}</ref> There is also substantial evidence that DNA damage accumulates with age in mammalian tissues, such as those of the brain, muscle, liver, and kidney (reviewed by Bernstein et al.<ref>{{cite book | vauthors = Bernstein H, Payne CM, Bernstein C, Garewal H, Dvorak K | date = 2008 | chapter = Chapter 1: Cancer and aging as consequences of un-repaired DNA damage.| title = New Research on DNA Damages | veditors = Kimura H, Suzuki A | publisher = [[Nova Science Publishers, Inc.]] | location = New York | pages = 1–47 | isbn = 978-1-60456-581-2 }}</ref> and see [[DNA damage theory of aging]] and [[DNA damage (naturally occurring)]]). One expectation of the theory (that DNA damage is the primary cause of aging) is that among species with differing maximum life spans, the capacity to repair DNA damage should correlate with lifespan. The first experimental test of this idea was by Hart and Setlow<ref>{{cite journal | vauthors = Hart RW, Setlow RB | title = Correlation between deoxyribonucleic acid excision-repair and life-span in a number of mammalian species | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 71 | issue = 6 | pages = 2169–73 | date = June 1974 | pmid = 4526202 | pmc = 388412 | doi = 10.1073/pnas.71.6.2169 | bibcode = 1974PNAS...71.2169H | doi-access = free }}</ref> who measured the capacity of cells from seven different mammalian species to carry out DNA repair. They found that [[nucleotide excision repair]] capability increased systematically with species longevity. This correlation was striking and stimulated a series of 11 additional experiments in different laboratories over succeeding years on the relationship of nucleotide excision repair and life span in mammalian species (reviewed by Bernstein and Bernstein<ref>{{cite book | vauthors = Bernstein C, Bernstein H | date = 1991 | title = Aging, Sex, and DNA Repair | publisher = Academic Press | location = San Diego | isbn = 978-0-12-092860-6 }}</ref>). In general, the findings of these studies indicated a good correlation between nucleotide excision repair capacity and life span. The association between nucleotide excision repair capability and longevity is strengthened by the evidence that defects in nucleotide excision repair proteins in humans and rodents cause features of premature aging, as reviewed by Diderich.<ref name=Diderich /> Further support for the theory that DNA damage is the primary cause of aging comes from study of [[Poly ADP ribose polymerase]]s (PARPs). PARPs are enzymes that are activated by DNA strand breaks and play a role in DNA base excision repair. Burkle et al. reviewed evidence that PARPs, and especially [[PARP-1]], are involved in maintaining mammalian longevity.<ref name="pmid15743677">{{cite journal | vauthors = Bürkle A, Brabeck C, Diefenbach J, Beneke S | title = The emerging role of poly(ADP-ribose) polymerase-1 in longevity | journal = The International Journal of Biochemistry & Cell Biology | volume = 37 | issue = 5 | pages = 1043–53 | date = May 2005 | pmid = 15743677 | doi = 10.1016/j.biocel.2004.10.006 }}</ref> The life span of 13 mammalian species correlated with poly(ADP ribosyl)ation capability measured in mononuclear cells. Furthermore, [[lymphoblastoid]] cell lines from peripheral blood lymphocytes of humans over age 100 had a significantly higher poly(ADP-ribosyl)ation capability than control cell lines from younger individuals.{{cn|date=November 2024}}
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)