Why cells make oxidants on purpose
Give trained volunteers high doses of vitamin C and E through a training block and, in several trials, they adapt less than the group swallowing placebo. If oxidants were only damage, that should be impossible.
Give trained volunteers high doses of vitamin C and E through a block of training, and something awkward happens in several of the trials that have tried it. The supplemented group adapts less than the group swallowing a dummy pill. Same sessions, same effort, smaller gain. If oxidants were only damage, that should be impossible.
By the end you will know where these reactive particles come from. You will also learn what “oxidative stress” properly means, and why more antioxidant is not automatically more health.
Where do reactive oxygen species come from?
First, the terms. When oxygen picks up stray electrons it forms unstable, reactive particles. Scientists call them reactive oxygen species. Some of them are made by accident. Mitochondria, the cell’s energy factories, pass electrons down a chain towards oxygen, and a fraction escape early. That is the accident everyone has heard about, and it is the smaller half of the story.
The rest is deliberate. A family of enzymes exists only to manufacture these reactive particles and release them where they are wanted. Immune cells carry them for killing invaders. Blood vessel walls and working muscle carry them for signalling. Much of the body’s oxidant load is not leakage at all: cells build dedicated enzymes whose only job is to make it.
Bodies do not build machinery to make a poison for no reason. So what is it for?
What does a cell do with an oxidant?
The workhorse is hydrogen peroxide. It is small enough to drift a short distance before reacting. When it reaches a target protein, it changes that protein’s shape by tweaking one sulphur-containing part of it. The change is reversible. Undo it and the switch flips back.
That is a signalling system, and it does real work. The burst of oxidants inside working muscle is part of what switches on the programmes that build new mitochondria, which is to say the training effect itself. Immune cells kill swallowed bacteria with a deliberate oxidative burst. In a rare inherited condition where that machinery is faulty, the result is severe repeated infection, so too little oxidant is a disease in its own right. Reactive oxygen species are among the body’s fastest signalling systems, and training adaptation, immune killing and ordinary growth signalling all run through them.
A signal only works if something can switch it off, and that machinery is nothing like the sponge it is usually described as.
Is antioxidant defence really a sponge?
No. It is more like a thermostat. One enzyme converts the most reactive particle into hydrogen peroxide. Others take that peroxide the rest of the way to water. Glutathione, the cell’s main protective molecule, is less used up than continuously recycled, drawing on energy from glucose. Antioxidant defence is not a sponge that soaks up oxidants; it is a regulated network that the oxidants themselves switch on.
The switch has a name. A sensor protein normally holds a control protein called NRF2 down and marks it for destruction. Oxidise that sensor and NRF2 is released. It enters the cell’s control centre and raises dozens of defence and repair genes for hours to days. A challenge today buys capacity tomorrow.
Which fixes the definition most popular writing gets wrong. Oxidative stress is not the presence of oxidants; it is production outrunning the defence that should be matching it. It happens when there is too much, in the wrong place, or for too long. Three variables, not one: how much, where, and how long.
Which brings us back to the trial at the top, and to what a gram of isolated antioxidant does to a system that already switches on its own defences.
Why is more antioxidant not more health?
In those training studies, the workout itself was largely unaffected. What shrank was the body’s response to it: the signalling that builds mitochondria and improves insulin sensitivity. Flooding the system with high-dose isolated antioxidants can quiet the very signal that asks the body to adapt, which is why several training trials found supplemented groups gaining less than the dummy-pill group.
Proven, but narrower than headlines suggest: several randomised trials of high-dose vitamin C and E during training reduced markers of mitochondrial adaptation, and some reduced actual gains. Other trials of similar design found no effect. Samples are small, doses differ, and none has run for years, so the molecular blunting is proven while its importance to any one person is still being studied. Separately, large trials of isolated antioxidant supplements have mostly not shown the benefit expected of them, and in one well-known trial beta-carotene given to smokers was linked to more lung cancer, not less. That is not an argument against nutrients, but against treating a signalling system bluntly.
Food behaves differently, and the reason is not sentimental. Food-source antioxidants act at small doses, are absorbed poorly, and work largely by nudging the body’s own defence network upward rather than neutralising anything directly. Many plant compounds are themselves mildly reactive. They register as a small challenge, NRF2 responds, and capacity goes up. That is close to the opposite of what a daily megadose does.
So if the supplement aisle is the wrong lever, what is the right one, and can any of it be measured?
What is worth doing, and what cannot yet be measured?
The useful levers move both sides of the balance. Regular training raises production briefly and defence durably. Sleep, blood glucose kept in a sensible range, and dealing with whatever drives long-term inflammation all lower the standing load. Sulphur-rich and colourful plants supply both the raw material for glutathione and the mild challenge that trains the network. Not smoking removes the largest avoidable oxidant exposure most people meet.
Measurement is where honesty is required. Research markers exist, and a few are reasonably well validated for studies. None has a reference range that reliably guides a decision about one individual, and results vary with the sample, the assay and the day. We do not yet have a routine clinical measure of oxidative status, and pretending otherwise sells tests rather than understanding.
When someone takes a high-dose antioxidant, the question worth asking is what it is for. Correcting a documented deficiency is one thing. A daily gram taken to feel generally protected is another, with the least evidence behind it and the most capacity to quiet a signal worth keeping.
- Much of the body’s oxidant load is made deliberately, by enzymes built for the job.
- They run training adaptation, immune killing and growth signalling; too little is also a disease.
- Defence is a network that oxidants switch on, not a sponge.
- Oxidative stress means production outrunning defence, not the mere presence of oxidants.
- High-dose isolated antioxidants can blunt adaptation; food-source ones mostly raise the body’s own defences.
- No routine test reliably reports a person’s oxidative status today.
Sparks, defences and the balance between them sit underneath almost everything else this field teaches, and the knowledge check will show how steadily you hold the balance level.
Deep DiveRedox in practice: reading oxidative status honestlyWork out what an oxidative stress panel can and cannot tell one person, why the glutathione ratio matters more than any total, and what stays actionable when no marker is trustworthy.