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 chronic 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.
Mitochondria are cellular structures that generate most of the energy needed by cells. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion -- joining with other mitochondria and exchanging material such as DNA.
While fusion is a well-known method for mitochondrial self- repair in many other tissues, most researchers assumed that the repair mechanism 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 fibers of the skeletal muscle cells that they have little opportunity to interact.
To investigate whether mitochondria in the muscle could indeed fuse to regenerate, 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 mingled.
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 interferes 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 gene 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.