Back نظرية الجذور الحرة والتشيخ Arabic Theorie der freien Radikale German Θεωρία της γήρανσης λόγω ελευθέρων ριζών Greek Théorie radicalaire du vieillissement French 노화의 자유 라디칼 이론 Korean Слободни радикали Macedonian Wolnorodnikowa teoria starzenia się Polish Свободнорадикальная теория старения Russian Слободни радикали Serbian Вільнорадикальна теорія старіння Ukrainian
 | This article needs more reliable medical references for verification or relies too heavily on primary sources. (May 2015) |  |
The free radical theory of aging states that organisms age because cells accumulate free radical damage over time.[1] A free radical is any atom or molecule that has a single unpaired electron in an outer shell.[2] While a few free radicals such as melanin are not chemically reactive, most biologically relevant free radicals are highly reactive.[3] For most biological structures, free radical damage is closely associated with oxidative damage. Antioxidants are reducing agents, and limit oxidative damage to biological structures by passivating them from free radicals.[4]
Strictly speaking, the free radical theory is only concerned with free radicals such as superoxide ( O2− ), but it has since been expanded to encompass oxidative damage from other reactive oxygen species (ROS) such as hydrogen peroxide (H2O2), or peroxynitrite (OONO−).[4]
Denham Harman first proposed the free radical theory of aging in the 1950s,[5] and in the 1970s extended the idea to implicate mitochondrial production of ROS.[6]
In some model organisms, such as yeast and Drosophila, there is evidence that reducing oxidative damage can extend lifespan.[7] However, in mice, only 1 of the 18 genetic alterations (SOD-1 deletion) that block antioxidant defences, shortened lifespan.[8] Similarly, in roundworms (Caenorhabditis elegans), blocking the production of the naturally occurring antioxidant superoxide dismutase has been shown to increase lifespan.[9] Whether reducing oxidative damage below normal levels is sufficient to extend lifespan remains an open and controversial question.
- ^ Hekimi S, Lapointe J, Wen Y. Taking a "good" look at free radicals in the aging process. Trends In Cell Biology. 2011;21(10) 569-76.
- ^ Erbas M, Sekerci H. "Importance of Free Radicals and Occurring During Food Processing". Serbest Radïkallerïn Onemï Ve Gida Ïsleme Sirasinda Olusumu. 2011: 36(6) 349–56.
- ^ Herrling T, Jung K, Fuchs J (2008). "The role of melanin as protector against free radicals in skin and its role as free radical indicator in hair". Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy. 69 (5): 1429–35. Bibcode:2008AcSpA..69.1429H. doi:10.1016/j.saa.2007.09.030. PMID 17988942.
- ^ a b Halliwell B (2012). "Free radicals and antioxidants: updating a personal view". Nutrition Reviews. 70 (5): 257–65. doi:10.1111/j.1753-4887.2012.00476.x. PMID 22537212.
- ^ Harman, D (1956). "Aging: a theory based on free radical and radiation chemistry". Journal of Gerontology. 11 (3): 298–300. doi:10.1093/geronj/11.3.298. hdl:2027/mdp.39015086547422. PMID 13332224.
- ^ Harman, D (1972). "A biologic clock: the mitochondria?". Journal of the American Geriatrics Society. 20 (4): 145–147. doi:10.1111/j.1532-5415.1972.tb00787.x. PMID 5016631. S2CID 396830.
- ^ Fontana, Luigi; Partridge, Linda; Longo, Valter D. (16 April 2010). "Extending Healthy Life Span—From Yeast to Humans". Science. 328 (5976): 321–326. Bibcode:2010Sci...328..321F. doi:10.1126/science.1172539. PMC 3607354. PMID 20395504.
- ^ Pérez VI, Bokov A, Remmen HV, Mele J, Ran Q, Ikeno Y, et al. (2009). "Is the oxidative stress theory of aging dead?". Biochimica et Biophysica Acta (BBA) – General Subjects. 1790 (10): 1005–14. doi:10.1016/j.bbagen.2009.06.003. PMC 2789432. PMID 19524016.
- ^ Van Rammsdonk, Jeremy M.; Hekimi, Siegfried (2009). Kim, Stuart K. (ed.). "Deletion of the Mitochondrial Superoxide Dismutase sod-2 Extends Lifespan in Caenorhabditis elegans". PLOS Genetics. 5 (2): e1000361. doi:10.1371/journal.pgen.1000361. PMC 2628729. PMID 19197346.