What Are Free Radicals & ROS?

Reviewed by SOMA HEALTH's Medical Research Team

Free radicals get blamed for everything from wrinkles to aging itself. The reality is more interesting. They are ordinary byproducts of the way your cells make energy, useful in small amounts and problematic in excess. Here is what free radicals and reactive oxygen species actually are, why aging mitochondria leak more of them, and where the evidence honestly stands.

The chemistry, in plain language

Atoms and molecules are most stable when their electrons are paired. A free radical is simply a molecule with an unpaired electron. That lone electron makes it chemically restless: it seeks to grab an electron from a neighboring molecule to become stable again. When it does, the molecule it took from becomes a radical itself, which can set off a short chain reaction. This reactivity is the whole story behind why free radicals matter, for better and for worse.

Reactive oxygen species, or ROS, is the broader umbrella term. It covers oxygen-based free radicals such as the superoxide anion and the hydroxyl radical, and it also includes some reactive oxygen molecules that are technically not radicals, such as hydrogen peroxide. Not every ROS has an unpaired electron, but all of them are reactive enough to participate in the same biology. In everyday wellness writing, free radicals and ROS are often used loosely as near-synonyms; the distinction matters mainly to chemists.

Where they come from: the energy connection

The dominant internal source of ROS is your own energy metabolism. Inside your mitochondria, the electron transport chain passes electrons down a series of protein complexes to ultimately combine with oxygen and make usable cellular energy. The system is highly efficient, but a small percentage of electrons slip out early, particularly at two of the complexes, and react with oxygen to form superoxide. That superoxide is then converted by enzymes into other species. In short, generating energy and generating ROS are two sides of the same reaction, which is why an aerobic life inevitably produces reactive byproducts.

External sources add to this baseline. Ultraviolet radiation, air pollution, cigarette smoke, certain drugs and metals, and intense exercise all raise ROS production. Some of these spikes are transient and even useful; others represent a chronic load. This is the same picture we describe in our explainer on oxidative stress, the state that develops when ROS production overwhelms your defenses.

Not the villain they are made out to be

It is tempting to treat free radicals as pure damage, but that misreads the biology. At controlled, everyday levels, ROS are essential signaling molecules. Immune cells deliberately produce bursts of them to destroy invading microbes. Muscle cells use ROS signals to adapt and grow stronger in response to training. Cells use them to regulate blood vessel tone and to switch certain genes on and off. A cell with too few ROS signals would function poorly. The concept that a mild, transient stress can trigger beneficial adaptation, sometimes called hormesis, is part of why moderate exercise is good for you even though it raises ROS in the moment.

So the honest framing is dose and duration. Low, well-managed levels of reactive molecules are normal and useful. Chronic excess, when production persistently exceeds your antioxidant and repair capacity, is the situation associated with cellular wear.

Your defenses against excess

Because ROS are unavoidable, your cells maintain a sophisticated counterbalance. Enzymes such as superoxide dismutase convert superoxide into less reactive molecules, while catalase and glutathione peroxidase neutralize hydrogen peroxide. Small-molecule antioxidants, including glutathione made inside your cells and vitamins C and E from your diet, mop up stray radicals. And when damage does occur, repair and recycling systems fix or clear the affected components. Under normal conditions, this network keeps pace with the steady trickle of ROS from metabolism.

Why aging mitochondria leak more

Here is the part most relevant to healthy aging. Over time, mitochondria accumulate damage and their internal machinery can become less precise. A less efficient electron transport chain tends to leak a larger fraction of its electrons, producing more ROS per unit of energy made. Those extra reactive molecules can, in turn, damage nearby mitochondria and other cell components, which can make them leak still more, a self-reinforcing loop that researchers have studied for decades. As a result, tissues that are dense in mitochondria and slow to renew, such as muscle and nerve, are of particular interest in aging research.

This is exactly why cellular housekeeping matters. The process called mitophagy identifies worn-out, leaky mitochondria and recycles them, allowing the cell to replace them with cleaner units. Supporting the turnover of aging mitochondria is a fundamentally different idea from simply swallowing more antioxidants; rather than mopping up ROS after the fact, it aims to keep the ROS-producing machinery itself in better shape. Our overview of mitochondrial health goes further on this.

Where urolithin A fits

Urolithin A is studied precisely for its role in supporting mitophagy. It is a gut postbiotic that your microbiome produces from ellagitannins found in pomegranates, walnuts, and berries, and notably, only some people's microbiomes convert it efficiently, which is one reason it is taken directly. The mechanism, promoting the recycling of worn mitochondria, was established largely in preclinical research: Ryu and colleagues, writing in Nature Medicine in 2016, showed urolithin A triggered mitophagy, extended lifespan in the worm C. elegans, and improved muscle measures in rodents. That work is foundational but is animal and cell-based, and does not by itself prove human benefit.

The human record is narrower and centers on mitochondrial support rather than ROS levels. A 2019 first-in-human study in Nature Metabolism (Andreux et al.) found urolithin A safe and well tolerated up to 1,000 mg per day, with a mitochondrial gene-expression signature. Randomized human trials reported benefits for muscle endurance in older adults (JAMA Network Open, 2022) and muscle strength in middle-aged adults (Cell Reports Medicine, 2022, at 500 and 1,000 mg). A 2025 randomized trial in Nature Aging reported support for the mitochondrial health of immune cells in midlife adults. A 2024 systematic review in Ageing Research Reviews concluded the human evidence is still emerging. Urolithin A is best understood as a mitochondrial-support ingredient, not an antioxidant and not a treatment for any condition.

Practical takeaways

You cannot and should not try to abolish free radicals. What helps is keeping the balance sensible: eat a variety of colorful plants for a broad antioxidant base, stay physically active so your defenses stay well trained, sleep enough, avoid smoking, moderate alcohol, and protect your skin from excess sun. Chasing very high doses of isolated antioxidant pills has not consistently beaten a whole-food pattern in research, and can even blunt some of exercise's benefits, another sign that balance matters more than brute force. For more on the ingredient discussed here, see our complete urolithin A guide, and if you are comparing options, our roundup of the best urolithin A gummies. This page is educational and is not medical advice; if you have a health condition or specific concern, please talk with your doctor.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. This guide is educational and is not a substitute for advice from a qualified healthcare provider.