Sastre Juan, Lloret Ana, Borrás Consuelo, Pereda Javier, García-Sala David, Droy-Lefaix Marie-Thérèse, Pallardó Federico V, Viña José
Departamento de Fisiologia, Facultad de Medicina, Universitat de València, Spain.
Cell Mol Biol (Noisy-le-grand). 2002 Sep;48(6):685-92.
According to the free radical theory of aging, oxygen-derived free radicals causes the age-associated impairment at the cellular and tissue levels. The mitochondrial theory of aging points to mitochondria, and specially mitochondrial DNA, as the major targets of free radical attack upon aging. Thus, oxidative damage to mtDNA accumulate with age in human and rodent tissues and also is inversely related to maximum life span of mammals. Mitochondrial deficits, such as a decrease in mitochondrial membrane potential, occur upon aging due to oxidative damage. The age-related mitochondrial oxidative stress may be prevented by late onset administration of certain antioxidants, such as Ginkgo biloba extract EGb 761. These antioxidants may also delay the physiological impairment associated with aging.
根据衰老的自由基理论,氧衍生的自由基会在细胞和组织水平上导致与年龄相关的损伤。衰老的线粒体理论指出线粒体,特别是线粒体DNA,是衰老过程中自由基攻击的主要目标。因此,mtDNA的氧化损伤在人类和啮齿动物组织中会随着年龄的增长而积累,并且与哺乳动物的最大寿命呈负相关。由于氧化损伤,衰老时会出现线粒体缺陷,如线粒体膜电位降低。通过后期给予某些抗氧化剂,如银杏叶提取物EGb 761,可以预防与年龄相关的线粒体氧化应激。这些抗氧化剂也可能延迟与衰老相关的生理损伤。