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2010年2月17日星期三

科學家發現老化的秘密

科學家發現老化的秘密
Scientists discover the secret of ageing

By Clive Cookson in London
Published: February 15 2010 23:00
Last updated: February 15 2010 23:00

One of the biggest puzzles in biology – how and why living cells age – has been solved by an international team based at Newcastle University, in north-east England.
在生物學中其中一個最大的難題 - 如何以及為什麼活體細胞會老化 - 已經被一支建基於英格蘭東北的紐卡素大學的國際組所拆解。
The answer is complex, and will not produce an elixir of eternal life in the foreseeable future.
答案是複雜的,和在可預見的未來不會產生仙丹般的永恆生命。
But the scientists expect better drugs for age-related illnesses, such as diabetes and heart disease, to emerge from their discovery of the biochemical pathway involved in ageing.
但科學家期望會有更好,與年齡有關的疾病 - 如糖尿病和心髒病 - 的藥物出現,在他們生化途徑涉及年齡老化的發現後。
The Newcastle team, working with the University of Ulm in Germany, used a comprehensive “systems biology” approach, involving computer modelling and experiments with cell cultures and genetically modified mice, to investigate why cells become senescent. In this aged state, cells stop dividing and the tissues they make up show physical signs of deterioration, from wrinkling skin to a failing heart.
那紐卡素大的隊伍與德國烏爾姆大學工作,用一個全面的“生物學系統”的方法,涉及用細胞培養和轉基因小鼠的電腦模型和試驗,調查為什麼有些細胞逐漸衰老。在這個上年紀狀態,細胞停止分裂和它們構成的組織顯示體徵惡化,由皮膚起皺至一個失敗的心。
The research, published by the journal Molecular Systems Biology, shows that when an ageing cell detects serious damage to its DNA – caused by the wear and tear of life – it sends out specific internal signals.
These distress signals trigger the cell’s mitochondria, its tiny energy-producing power packs, to make oxidising “free radical” molecules, which in turn tell the cell either to destroy itself or to stop dividing. The aim is to avoid the damaged DNA that causes cancer.

The Newcastle discovery plays down the role of telomeres, the protective tips on the ends of human chromosomes, which gradually become shorter as we grow older.
“There has been a huge amount of speculation about how blocking telomere erosion might cure ageing and age-related diseases,” said Tom Kirkwood, director of Newcastle’s Institute of Ageing and Health. “The telomere story has over-promised and the biology is more complicated.”
He added: “Our breakthrough means that we stand a very much better chance of making a successful attack on age-related diseases while at the same time avoiding the risk of unwanted side-effects like cancer.”
His colleague Thomas von Zglinicki emphasised caution in the research’s next stage – to investigate ways to prevent cellular senescence.
“It is absolutely essential to tread carefully in trying to alter processes that cause cells to age, because the last thing we want is to help age-damaged cells from breaking out to become malignant,” said Mr von Zglinicki.
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