Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Brazil.
Ageing Res Rev. 2013 Jan;12(1):22-8. doi: 10.1016/j.arr.2012.03.009. Epub 2012 Apr 6.
Mitochondrial energy metabolism and mitochondrially-derived oxidants have, for many years, been recognized as central toward the effects of aging. A body of recent work has focused on the relationship between mitochondrial redox state, aging and dietary interventions that affect lifespan. These studies have uncovered mechanisms through which diet alters mitochondrial metabolism, in addition to determining how these changes affect oxidant generation, which in itself has an impact on mitochondrial function in aged animals. Many of the studies conducted to date, however, are correlative, and it remains to be determined which of the energy metabolism and redox modifications induced by diet are central toward lifespan extent. Furthermore, dietary interventions used for laboratory animals are often unequal, and of difficult comparison with humans (for whom, by nature, no long-term sound scientific information on the effects of diet on mitochondrial redox state and aging is available). We hope future studies will be able to mechanistically characterize which energy metabolism and redox changes promoted by dietary interventions have positive lifespan effects, and translate these findings into human prevention and treatment of age-related disease.
线粒体能量代谢和线粒体衍生的氧化剂多年来一直被认为是衰老效应的核心。最近的一系列研究集中在线粒体氧化还原状态、衰老和影响寿命的饮食干预之间的关系上。这些研究揭示了饮食改变线粒体代谢的机制,此外还确定了这些变化如何影响氧化剂的产生,而氧化剂的产生本身会对老年动物的线粒体功能产生影响。然而,迄今为止进行的许多研究都是相关的,仍然需要确定饮食引起的能量代谢和氧化还原修饰中,哪些是与寿命长短密切相关的。此外,用于实验室动物的饮食干预通常是不平等的,并且难以与人类进行比较(因为从本质上讲,关于饮食对线粒体氧化还原状态和衰老的影响,人类没有长期的可靠科学信息)。我们希望未来的研究能够从机制上描述饮食干预促进的哪些能量代谢和氧化还原变化具有延长寿命的效果,并将这些发现转化为人类预防和治疗与年龄相关的疾病的方法。