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WASHINGTON, April 21 (Xinhua) -- U.S. researchers said Monday that muscle weakness from long-term alcoholism may be due to an inability of mitochondria, the powerhouses of cells, to self- repair.
In research conducted with rats, the researchers found evidence that chronic1 heavy alcohol use affects a protein involved in mitochondrial repair and muscle regeneration.
"The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development," George Koob, director of the U.S. National Institute on Alcohol Abuse and Alcoholism that funded the study, said in a statement.
Researchers identify why alcoholism causes muscle weakness
Mitochondria are cellular3 structures that generate most of the energy needed by cells. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion4 -- joining with other mitochondria and exchanging material such as DNA5.
While fusion is a well-known method for mitochondrial self- repair in many other tissues, most researchers assumed that the repair mechanism6 is unlikely to occur in skeletal muscle, which relies constantly on mitochondria for power. The reason is that mitochondria are squeezed so tightly in between the packed fibers7 of the skeletal muscle cells that they have little opportunity to interact.
To investigate whether mitochondria in the muscle could indeed fuse to regenerate8, researchers from the Thomas Jefferson University created a system to tag the mitochondria in skeletal muscle of rats with two different colors and then watch if they mingled9.
The study showed for the first time that the mitochondrial fusion does occur in the skeletal muscle cells, the researchers said.
They were also able to identify a key protein called mitofusin 1 (Mfn1) fusion proteins in the process and show that alcoholism interferes10 with the process.
In rats that were given an alcohol diet, Mfn1 levels decreased as much as 50 percent while other fusion proteins were unchanged. This decrease in Mfn1 was coupled with a dramatic decrease in mitochondrial fusion. When Mfn1 returned to normal, mitochondrial fusion did as well.
"That alcohol can have a specific effect on this one gene2 involved in mitochondrial fusion suggests that other environmental factors may also alter specifically mitochondrial fusion and repair," said lead author Gyorgy Hajnoczky, professor of the Thomas Jefferson University.
He also suggested that knowing the proteins involved in mitochondrial fusion may aid in drug development for alcohol- related muscle weakness.
The findings were published in the U.S. Journal of Cell Biology.
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1 chronic | |
adj.(疾病)长期未愈的,慢性的;极坏的 | |
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2 gene | |
n.遗传因子,基因 | |
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3 cellular | |
adj.移动的;细胞的,由细胞组成的 | |
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4 fusion | |
n.溶化;熔解;熔化状态,熔和;熔接 | |
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5 DNA | |
(缩)deoxyribonucleic acid 脱氧核糖核酸 | |
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6 mechanism | |
n.机械装置;机构,结构 | |
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7 fibers | |
光纤( fiber的名词复数 ); (织物的)质地; 纤维,纤维物质 | |
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8 regenerate | |
vt.使恢复,使新生;vi.恢复,再生;adj.恢复的 | |
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9 mingled | |
混合,混入( mingle的过去式和过去分词 ); 混进,与…交往[联系] | |
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10 interferes | |
vi. 妨碍,冲突,干涉 | |
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