The damage caused by free radicals has been known for a long time. However, a recent study shows that they also enhance regeneration.
Let’s start at the beginning: all matter is composed of atoms. The nucleus of an atom is orbited by electrons, like our earth is orbited by satellites. When an atom loses one of its electrons under certain conditions, it becomes a “free radical.”
Electrons are their obsession and they are trying to become complete again. The electrons are thus “torn” from adjacent molecules, causing them to be damaged.
The body’s cells also undergo metabolic processes, where free radicals are formed when electrons are coupled and decoupled.

Free radicals aren’t just harmful

Due to their electron raid, scientists regarded these free radicals, also called ROS (reactive oxygen species), as “harmful.” Researchers have discovered, however, that ROS can also be beneficial in the right amounts.
The research group around Dr. Simone Di Giovanni (UCL London) has now discovered that free radicals are needed for axonal regeneration in an experimental model.

Why? How do they work?

This is where it gets complicated: an injury is always accompanied by inflammation and thus an accumulation of inflammatory cells and the production of ROS. The team led by Simone di Giovanni has demonstrated that macrophages (a type of inflammatory cell) release oxidative complexes packed in membranes. Axons that have been injured absorb these substances. Axons transport the proteins back into the body of the cell where they are unpacked. As they do so, they oxidize PTEN, an inhibitor of regeneration. As a result of the ROS, PTEN is inactivated, which stimulates cellular regeneration.

How do you interpret that? What’s next?

Axon outgrowth after injury is dependent on the transport of free radicals from inflammatory cells back to the nucleus through the axons. Using this knowledge, researchers can explore new therapeutic approaches that might also be helpful for spinal cord injuries.
“As usual, everything in moderation. Free radicals are important signal substances in normal conditions, but their excessive levels or long-term increase can lead to disease,” explains professor H*kan Westerblad, who led the study.
When the body is under stress, the sympathetic nervous system stimulates receptors called beta-adrenergic receptors on the surface of heart muscle cells. Phosphorylation of proteins is one of the changes inside the cells as a result of this. Thus, the contractions of the cells become stronger and the heart beats faster.
In the current study, the scientists demonstrate that stimulation of beta-adrenergic receptors also increases the production of free radicals in the mitochondria of the cells, and these free radicals then contribute to stronger contractions of the cells. Researchers found that beta-adrenergic stimulation of the heart muscle cells disappeared when cells were exposed to antioxidants.
The findings could contribute to a better understanding of various types of heart disease, as they reveal a previously unknown mechanism that controls force production in the heart.
Free radicals play a big role in the ability of the heart to pump more blood under stress, according to Håkan Westerblad. Chronically high levels of free radicals may also contribute to heart failure when persistent stress is present.