Falone S, Santini S Jr, Cordone V, Grannonico M, Cacchio M, Di Emidio G, Tatone C, Amicarelli F
Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy.
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.
Oxid Med Cell Longev. 2016;2016:3837623. doi: 10.1155/2016/3837623. Epub 2016 Dec 28.
Population aging results in urgent needs of interventions aimed at ensuring healthy senescence. Exercise often results in healthy aging, yet many molecular mechanisms underlying such effects still need to be identified. We here investigated whether the age-dependent accumulation of oxidative and methylglyoxal- (MG-) related molecular damage could be delayed by moderate exercise in the mouse ovary, an organ that first exhibits impaired function with advancing age in mammals. CD1 female mice underwent two- or four-month treadmill-based running through the transition from adult to middle age, when ovaries show signs of senescence, and markers of protection against reactive oxygen species (ROS) and MG were measured. The long-term exercise reduced the protein oxidative damage in the ovaries ( < 0.01), and this was linked to the preservation of the glutathione peroxidase protection against ROS ( < 0.001), as well as to the increased glutathione availability ( < 0.001). Conversely, even though the age-related deactivation of the MG-targeting systems was partially prevented by the long-term running programme ( < 0.001), exercised mice were not protected from the age-dependent glycative burden. In summary, lately initiated regular and moderate exercise limited some changes occurring in the ovaries of middle-aged mice, and this might help to develop nonpharmacological cointerventions to reduce the vulnerability of mammalian ovaries towards redox dysfunctions.
人口老龄化导致迫切需要采取干预措施以确保健康衰老。运动通常会带来健康老龄化，但这种效应背后的许多分子机制仍有待确定。我们在此研究了在小鼠卵巢中，与氧化和甲基乙二醛（MG）相关的分子损伤随年龄增长的积累是否可以通过适度运动来延缓，卵巢是哺乳动物中随着年龄增长首先出现功能受损的器官。CD1雌性小鼠在从成年过渡到中年期间，即卵巢出现衰老迹象时，进行了为期两个月或四个月的基于跑步机的跑步，并测量了抗氧化应激（ROS）和MG的保护标志物。长期运动减少了卵巢中的蛋白质氧化损伤（<0.01），这与谷胱甘肽过氧化物酶对ROS的保护作用的保留有关（<0.001），以及谷胱甘肽可用性的增加（<0.001）。相反，尽管长期跑步计划部分阻止了与年龄相关的MG靶向系统的失活（<0.001），但运动小鼠并未免受年龄依赖性糖基化负担的影响。总之，近期开始的规律适度运动限制了中年小鼠卵巢中发生的一些变化，这可能有助于开发非药物联合干预措施，以降低哺乳动物卵巢对氧化还原功能障碍的易感性。
