The Mitochondrial Free Radical Theory of Aging: A Critical View

• DOI: 10.2174/1874609810801010010
• Publication Date: 2010-01-09T13:52:49Z
• Authors: Alberto Sanz; Rhoda K.A. Stefan...
• Keywords: Mitochondrial ROS; Life span

The Mitochondrial Free Radical Theory of Aging (MFRTA) proposes that mitochondrial free radicals, produced as by-products during normal metabolism, cause oxidative damage. According to MFRTA, the accumulation this damage is main driving force in aging process. Although widely accepted, theory remains unproven, because evidence supporting it largely correlative. For example, long-lived animals produce fewer radicals and have lower levels their tissues. However, does not prove radical generation determines life span. In fact, longest-living rodent -Heterocephalus glaber- produces high has significant proteins, lipids DNA. At its most orthodox MFRTA these DNA (mtDNA) turn provoke mutations alter function (e.g. ATP production). this, mtDNA negatively correlates with maximum span mammals. contrast predictions, do decrease longevity mice. Moreover, mice alterations polymerase gamma (the polymerase) accumulate 500 times higher point without suffering from accelerated aging. Dietary restriction (DR) only non-genetic treatment clearly increases mean caloric restricted reactive oxygen species (mtROS). DR alters more than production decreases insulin signalling) therefore increase cannot be exclusively attributed a mtROS generation. Thus, moderate exercise similar changes increasing summary, available data concerning role control are contradictory, MFRTA. way test by specifically decreasing altering other physiological parameters signalling). If true producing must ability live much longer experimental controls. Keywords: Aging, comparative biology aging, mitochondria, species, damage, dietary restriction,