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每日科学（10.31,2011）——较少的摄入卡路里，年华会放慢脚步，并且诸如癌症和2型糖尿病等与年龄相关的疾病的进展也会被延迟下来。越早减少卡路里的摄入，效果越显著。如今哥登堡大学的研究人员已经确认了一种在保持青春起关键作用的酶。 "We are able to show that caloric restriction slows down aging by preventing an enzyme, peroxiredoxin, from being inactivated. This enzyme is also extremely important in counteracting damage to our genetic material," says Mikael Molin of the Department of Cell and Molecular Biology. “我们已能够表明限制卡路里摄入能够通过阻断一种过氧化物酶的灭活而保持青春。这种酶对阻断人类基因损伤也有十分重要的作用。”细胞分子生物学家麦克穆林说道。 By gradually reducing the intake of sugar and proteins, without reducing vitamins and minerals, researchers have previously shown that monkeys can live several years longer than expected. The method has also been tested on everything from fishes and rats to fungi, flies and yeasts with favourable results. Caloric restriction also has favourable effects on our health and delays the development of age-related diseases. Despite this, researchers in the field have found it difficult to explain exactly how caloric restriction produces these favourable effects. 通过逐渐的减少糖类和蛋白质的摄入，同时不减少维生素和谷物类的量，研究人员预先的发现猴子能够比预想的寿命要长几年。类似的实验从鱼类和老鼠一直到真菌、果蝇、酵母，均取得了预想的结果。限制卡路里对健康有正面的作用同时延缓年龄相关疾病的进展。尽管如此，研究者们还是很难解释这种正面效应的确切机理。 Using yeast cells as a model, the research team at the University of Gothenburg has successfully identified one of the enzymes required. They are able to show that active peroxiredoxin 1, Prx1, an enzyme that breaks down harmful hydrogen peroxide in the cells, is required for caloric restriction to work effectively. 哥登堡大学的研究团队将酵母细胞作为模型，成功的确认出这种所需的酶。他们已经证明出活性过氧化物酶1（prx1），一种能够将细胞内有害的过氧化氢分解的酶类，正是此正面效应的所需酶类。 The results, which have been published in the journal Molecular Cell, show that Prx1 is damaged during aging and loses its activity. Caloric restriction counteracts this by increasing the production of another enzyme, Srx1, which repairs Prx1. Interestingly, the study also shows that aging can be delayed without caloric restriction by only increasing the quantity of Srx1 in the cell. Repair of the peroxiredoxin Prx1 consequently emerges as a key process in aging. 这项成果已发表在分子细胞学杂志上，表明了过氧化物酶1会随着年龄的增长而遭到破坏并失去活性。卡路里的限制则能通过增加另一种prx1酶修复酶srx1的生成而抵消这种破坏。有意思的是，这项研究表明保持青春也可以直接通过增加srx1酶的量（非限制卡路里）而实现。因此，prx1的修复酶作为保持青春的关键酶浮出水面。 "Impaired Prx1 function leads to various types of genetic defects and cancer. Conversely, we can now speculate whether increased repair of Prx1 during aging can counteract, or at least delay, the development of cancer." “prx1酶功能的破坏将导致各种类型的基因缺陷和恶性肿瘤。相反，我们如今已经可以推测这种prx1修复酶的增加是否能抵消至少延缓肿瘤的产生。” Peroxiredoxins have also been shown to be capable of preventing proteins from being damaged and aggregating, a process that has been linked to several age-related disorders affecting the nervous system, such as Alzheimer's and Parkinson's. The researchers are accordingly also considering whether stimulation of Prx1 can reduce and delay such disease processes. 已经有研究表明抗氧化蛋白能够防止蛋白质的破坏和凝聚,而此过程与多种年龄相关性神经系统功能失调相联系，例如老年痴呆症和帕金斯综合症。因此，研究者们也开始关注是否prx1的激活也能够降低或延缓这类疾病的病程。 |
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