据美国《每日科学》10月31日报道，瑞典歌德堡大学日前研究发现，人们减少摄取卡路里不仅有助于延缓衰老，还有利于推迟糖尿病、癌症等老年病的患病期，且越早减少卡路里的摄入量效果越明显。
该研究的负责人歌德堡大学细胞分子生物学专家米卡埃尔·莫林介绍说：“研究表明，人体内有一种酶是延缓人体老化的关键因素，它叫氧化还原酶 （peroxiredoxin），减少卡路里的摄取量能够有效保持这种酶的活性。不仅如此，这种酶对人体还有个至关重要的作用，它可以有效保护我们体内的 基因物质。”
虽然研究人员目前尚不能解释这种“延年益寿大法”的确切原理，但就目前掌握的研究结果来开，具备活性的过氧还原酶可以降 解人体细胞内的有害物质过氧化氢，而这种酶只有当人体的卡路里摄入量在得到一定限制时才会很好的发挥功效。随着人们年龄的增长，体内的过氧还原酶会逐渐遭 到破坏，失去活性，但有一种酶可以对其进行修复，它就是Srx1，减少卡路里的摄取量会促使人体增加Srx1的产量。
据悉，研究者在实验中以猴子为实验对象，通过逐渐降低糖和蛋白的摄入量，保持维生素和矿物质的摄入量，这些猴子的寿命明显延长了数年。研究者随即在鱼类、啮齿类、昆虫、菌类等多个物种上进行了相同实验，都取得良好效果。
研究人员目前正在检验过氧还原酶是否也可以减少或延缓人类的神经类疾病，因为该种酶同时也对人类体内的蛋白质有保护作用，其保护人体蛋白质的过程又与一些神经系统类的老年病息息相关。
By consuming fewer calories, aging can be slowed down and the development of age-related diseases such as cancer and type 2 diabetes can be delayed. The earlier calorie intake is reduced, the greater the effect. Researchers at the University of Gothenburg have now identified one of the enzymes that hold the key to the aging process…
“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.
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.
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.
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.
“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.”
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.
http://www.sciencedaily.com/releases/2011/10/111031215938.htm
