According to the researchers, it was previously known that chemotherapy drugs can affect the mitochondria within cells, which can cause the loss of muscle tissue via a process called oxidative stress.
In their new study, the researchers studied three different chemotherapy drugs in cultured muscle cells at levels too low to trigger oxidative stress. They found that the muscle cells were still affected by the lower levels of drugs -- this time by interfering with the process that builds muscle, called protein synthesis.
Gustavo Nader, associate professor of kinesiology, said that while the findings need to be confirmed in humans, they could have implications for cancer treatment in the future.
"Eventually, it may be that the implementation of cancer treatments should consider that even at low doses that do not cause oxidative stress, some chemotherapy drugs may still promote the loss of muscle tissue," Nader said. "The tumor is already making you weak, it's contributing to the loss of muscle mass, and the chemo drugs are helping the tumor to accomplish that."
Additionally, Nader said the results -- recently published in the American Journal of Physiology -- Cell Physiology -- also have the potential to change how health care professionals think about the ways chemotherapy affects the body.
"For a long time, people thought the problem with chemo and muscle loss was an issue with degrading the proteins that already existed in the muscle," Nader said. "So, a lot of research and treatments in the past had the goal of preventing protein degradation. But our study points to there also being a problem with protein synthesis, or the building of new muscle proteins, as well."
Nader said that in addition to having implications for chemotherapy treatment, the findings could also ultimately change the way health care professionals think about other, pharmaceutical cancer treatments and programs.
Bin Guo, Devasier Bennet, Daniel J. Belcher, et al. Chemotherapy agents reduce protein synthesis and ribosomal capacity in myotubes independent of oxidative stress, American Journal of Physiology-Cell Physiology (DOI: 10.1152/ajpcell.00116.2021)