Loft S, Astrup A, Buemann B, Poulsen H E
Department of Pharmacology, University of Copenhagen, Denmark.
FASEB J. 1994 May;8(8):534-7. doi: 10.1096/fasebj.8.8.8181672.
Generation of reactive oxygen species from mitochondrial respiration has been proposed as an important determinant of longevity and cumulative cancer risk. Interspecies correlations and animal calorie restriction studies of metabolic rate and oxidative DNA damage support this notion. In the present study we have demonstrated a close association between oxidative DNA damage as assessed by the urinary excretion of 8-oxo-7,8-dihdro-2'-deoxyguanosine (8-oxodG) and oxygen consumption in 33 healthy premenopausal women (r = 0.64; p = 0.00007). In the 12 women who smoked, 8-oxodG excretion was increased by 35%, although oxygen consumption increased only 10% compared with the 21 nonsmoking women. Apparently, the rate of oxidative DNA damage relates to mitochondrial respiration in humans and is aggravated by smoking.
线粒体呼吸产生的活性氧被认为是寿命和累积癌症风险的重要决定因素。种间相关性以及动物热量限制研究中的代谢率和氧化性DNA损伤支持了这一观点。在本研究中，我们证实在33名健康的绝经前女性中，通过尿中8-氧代-7,8-二氢-2'-脱氧鸟苷（8-氧代脱氧鸟苷，8-oxodG）排泄量评估的氧化性DNA损伤与耗氧量之间存在密切关联（r = 0.64；p = 0.00007）。在12名吸烟女性中，8-氧代脱氧鸟苷排泄量增加了35%，尽管与21名不吸烟女性相比，耗氧量仅增加了10%。显然，氧化性DNA损伤的速率与人类线粒体呼吸有关，并且吸烟会加剧这种损伤。
