老化會伴隨著與年齡相關(guān)的各種疾病以及身體外貌的變化,，而且在不同的人身上有著不同的速度,?？茖W(xué)家之前已經(jīng)將老化歸咎于生命中累積的細胞損耗,，但是并未考慮可能遺傳的老化速度?，F(xiàn)在,，一個來自瑞典卡羅林斯卡醫(yī)學(xué)院和德國馬克斯普朗克生物研究所的研究團隊已經(jīng)發(fā)現(xiàn),，線粒體中的受損DNA在一定程度上會控制實驗鼠的老化速度。

研究人員聲稱,，遺傳自母體的線粒體DNA或許會決定你的老化速度,。

馬克斯普朗克研究所的研究人員Nils-Göran Larsson說道：“我們之前證實的是線粒體DNA隨著動物老化會出現(xiàn)損傷。但是現(xiàn)在,，我們也發(fā)現(xiàn)一些損傷在出生時就已經(jīng)存在,，而且是從母親遺傳給了孩子。”線粒體DNA與存在于細胞核的DNA不同,，它們遺傳自雙親,，而線粒體DNA只來源于母體基因。Larsson在一份聲明中說道,，研究人員發(fā)現(xiàn)線粒體DNA隨著時間出現(xiàn)損傷,，細胞的能量制造逐漸變得殘缺而且促使老化出現(xiàn)。
 
為了確定線粒體DNA損傷對老化產(chǎn)生的效果,，研究團隊飼養(yǎng)了伴有各種不同程度DNA損傷的實驗室老鼠,，而且通過測量體重、生育能力和紅細胞總數(shù)等健康條件來估算它們的老化速度,。研究團隊發(fā)現(xiàn),，DNA損傷程度高的老鼠會出現(xiàn)較低的健康水平。然而線粒體DNA損傷與環(huán)境壓力導(dǎo)致老化之間的相對關(guān)系尚不清楚,。
 
Larsson聲稱：“雖然這些發(fā)現(xiàn)有可能暗示著人類的老化速度,，但是我們也需要進行額外的研究,。我們使用了一系列的實驗條件來確定我們的研究結(jié)果，而且我們認為它們適用于人類,，但是這當然需要通過人類試驗進行證實,。”研究團隊的下一個計劃就是研究損傷線粒體DNA在老化中的相對角色，他們將通過基因工程減少突變線粒體DNA的遺傳水平,。Larsson聲稱,，他們希望他們的研究能夠為其它研究人員提供研究的基礎(chǔ)。(生物谷 Bioon.com)

生物谷推薦的英文內(nèi)容

A mother’s genes influence her child’s ageing

As we grow older, not only the function of organs slows down. Also on a cellular level more and more damages occur. One reason is that DNA errors accumulate which cause defective cells. Now a team of researchers lead by Nils-Göran Larsson at the Max Planck Institute for Biology of Ageing in Cologne has shown that ageing is determined not only by the accumulation of DNA damage that occurs during lifetime but also by damage that we acquire from our mothers. In a study on mice, the researchers have shown that mutations of maternally inherited mitochondrial DNA influence the offspring’s ageing process starting from birth.

Ageing is a complex process, in the course of which more and more damage accumulates within the bodies’ tissues, cells and molecules – with serious consequences: Organs lose their function and mortality risk increases. Why some people age faster than others has many reasons that are still unsolved. However, damage that occurs within the mitochondria – the cell’s powerhouses – seems to be of particular importance for ageing.

“The mitochondrion contains its own DNA, the so-called mitochondrial DNA or mtDNA, which changes faster than the DNA in the nucleus, and this has a significant impact on the ageing process,” says Nils-Göran Larsson, Director at the Max Planck Institute for Biology of Ageing in Cologne and scientist at the Karolinska Institute in Stockholm. Together with Lars Olson, also a scientist at the Karolinska Institute, he has led the study.

“Many mutations in the mitochondria gradually disable the cell’s energy production.” Contrary to previous findings, not only mutations that accumulate during lifetime play a role: “Surprisingly, we discovered that our mother’s mitochondrial DNA seems to influence our own ageing,” says James Stewart, a researcher in Larsson’s department. “If mice inherit mtDNA with mutations from their mother, they age more quickly.” Thus, some of the mutations that cause ageing are already present at birth.

In ageing research, mitochondria have been scrutinized by researchers for a long time already. The mitochondria in a cell contain thousand of copies of a circular DNA genome. These encode, for instance, proteins that are important for the enzymes of the respiratory chain. Whereas the DNA within the nucleus comes from both parents, the mitochondrial DNA only includes maternal genes, as mitochondria are transmitted to offspring via the oocyte and not via sperm cells. As the numerous DNA molecules within a cell’s mitochondria mutate independently from each other, normal and damaged mtDNA molecules are passed to the next generation.

To examine which effects mtDNA damage exerts on offspring, researchers used a mouse model. Mice that inherited mutations of mtDNA from their mother not only died quicker compared to those without inherited defects, but also showed premature ageing effects like reduced body mass or a decrease in male’s fertility. Moreover, these rodents were prone to heart muscle disease.

As the researchers discovered, mutations of mtDNA not only can accelerate ageing but also impair development: In mice that, in addition to their inherited defects, accumulated mutations of mtDNA during their lifetime, researchers found disturbances of brain development. They conclude that defects of mtDNA that are inherited and those that are acquired later in life add up and finally reach a critical number.

“Our findings shed light on the ageing process and strongly suggest that the mitochondria play a key role in ageing. They also show that it is important to reduce the number of mutations,” says Larsson. However, the question of whether it is possible to affect the degree of mtDNA damage through, for example, lifestyle intervention is yet to be investigated. In the future, the scientists want to investigate whether a reduced number of mutations can actually increase lifespan in model organisms such as fruit flies and mice.