Two words used constantly and defined almost never. Both have exact chemical meanings, and those are the useful ones.
~12 min read
Oxidation is the loss of electrons. That is the entire definition — no damage in it, no implication of anything going wrong. A molecule that hands an electron to another has been oxidised, and the word says nothing more.
The name came from the first reactions of this kind chemists studied, which all involved oxygen: iron rusting, fat going rancid in a cupboard. Oxygen turned out not to be the necessary ingredient. What those reactions shared was one substance handing electrons to another, and oxygen was simply the most available taker — at an electronegativity of 3.44, one of the most electron-hungry atoms there is, the same figure that pulls a carbon–oxygen bond off balance.
Electrons are never lost into nothing. Every oxidation is matched by a reduction — one gives, another receives — so the pair counts as one event, a redox reaction. Your body runs on exactly this; every calorie you use is electrons moving down a chain. Oxidation is not the problem, then. The problem is what a molecule becomes when it is left one electron short of a pair.
In atoms and bonding you met the rule that makes this subject predictable: electrons are stable in pairs. A shared pair is a covalent bond; an unshared pair sits out on an oxygen and bends a water molecule. Pairing is what electrons settle into when they can.
A free radical is a molecule carrying an electron with no partner, marked by chemists with a dot — •OH, or O2•− where it also carries a charge. Not a poison, not an intruder: an unfinished arrangement, which finishes itself the fastest way available, by taking an electron from whatever is nearest.
Superoxide, O2•−
Oxygen that has picked up one extra electron. The most common radical a cell makes, and the starting point for the others.
Hydrogen peroxide, H2O2
Not a radical — its electrons are all paired. It belongs here because it is stable enough to cross a membrane, and can be split into radicals when it arrives.
Hydroxyl radical, •OH
The most reactive of the set by a wide margin. Published estimates put its lifetime in water near a nanosecond, so it reacts with whatever sits a molecule or two from where it formed.
Peroxyl radical, ROO•
What a fatty acid becomes after being attacked and then meeting an oxygen molecule. This is the species that carries a chain through a membrane.
Now the part the popular account leaves out. The molecule a radical takes from is itself left short — a radical now, doing the same to its neighbour. Oxidative change is a chain rather than an event: one radical inside a membrane can alter a long run of fatty acids before anything stops it. The run ends when two radicals meet, or when something absorbs the change without passing it on.
Diagram to come
Three stacked rows, one per stage of a chain, drawn as skeletal structures at one consistent scale so a reader can follow a single hydrogen atom moving. Row one, initiation: a length of polyunsaturated fatty acid chain with two double bonds and the single carbon between them clearly marked; a hydroxyl radical approaching, drawn with its unpaired electron as a visible dot; a curved arrow showing one hydrogen leaving that middle carbon; products drawn to the right as water plus the fatty acid now carrying a dot on that carbon. Row two, propagation: the same carbon radical meeting an O2 molecule to become a peroxyl radical with the dot on the terminal oxygen; that peroxyl radical then pulling a hydrogen from a second, untouched fatty acid drawn below it, which is left carrying a dot of its own; a bold arrow looping from that new radical back to the start of the row so the cycle is unmistakable, with a counter beside the loop reading one event, many molecules altered. Row three, termination: the same peroxyl radical meeting a phenol drawn as a six-carbon aromatic ring with an –OH group; the hydroxyl hydrogen transferring across; and — the single most important thing in the figure — the resulting phenoxyl radical drawn NOT with a dot on one atom but with a soft shaded cloud spread evenly around the whole ring, with the chain arrow beside it drawn broken or crossed to show it stops here. The visual contrast between a concentrated dot in rows one and two and a spread cloud in row three carries the whole lesson.
A radical does not attack a fatty acid at random. It takes the hydrogen cheapest to remove, and that cost is measurable: the bond dissociation energy of the carbon–hydrogen bond.
Published tables put an ordinary carbon–hydrogen bond in a saturated chain at roughly 410 to 420 kilojoules per mole. Next to one double bond it falls to around 360, because the radical left behind can spread its unpaired electron into that bond. Between two double bonds, with a spread on each side, it falls again — near 315 in most published sets.
That hundred-kilojoule gap is why polyunsaturated fats oxidise and saturated ones largely do not. Count the positions: a fatty acid with two double bonds has one carbon between them, and DHA, with six, has five. It is fragile not because it is delicate but because it offers five cheap hydrogens, and a chain needs one. The same arithmetic runs on your shelf, where limonene — 60 to 75 per cent of lemon — carries two.
The popular story has radicals arriving from outside — smoke, pollution, modern living. Some do. Most are made by you, deliberately or as an unavoidable cost of metabolism.
Mitochondria, every second you are awake
Energy production moves electrons down a controlled sequence of carriers, and a few slip off early onto oxygen to form superoxide. Published estimates put the leak at a fraction of one per cent up to a couple of per cent of the oxygen a cell consumes — small as a percentage, enormous as a total.
Immune cells, on purpose
Certain white cells make radicals as a tool, in a burst, inside the compartment where they have enclosed what they are breaking down. Normal defence working correctly.
Ultraviolet light, smoke, and the liver at work
A photon with enough energy knocks an electron out of a molecule in the skin’s outer layers. Smoke arrives with radicals already made. And the liver produces them while processing ordinary compounds.
Then the fact that corrects the popular picture most: radicals are used as signals. Hydrogen peroxide carries messages between cells, and the adaptation a muscle makes to hard exercise depends partly on a transient rise in radical signalling. A cell unable to make these species would not be a cleaner cell. It would be one that had lost part of its vocabulary.
Radicals are not the enemy
A body that suppressed radical production completely would work less well, not better. What the literature describes is not radicals against the body but a balance: the rate they are produced, against the rate the body handles them. Oxidative stress names production outrunning handling — a statement about a ratio.
Stopping a chain takes a molecule that can do two things at once: give up an electron easily — usually as a whole hydrogen atom, proton and electron together — and stay stable afterwards. One that gives easily and then turns reactive itself has not ended the chain. It has joined it.
The second requirement is the interesting one, and you already have the chemistry. In functional groups a phenol was a hydroxyl sitting directly on an aromatic ring, and the ring pulled electron density away so the oxygen held its hydrogen loosely. Run that in reverse. Once the hydrogen has gone, the ring does not leave the unpaired electron parked on the oxygen; it spreads it across the shared cloud that makes the ring aromatic. An electron spread over six carbons and an oxygen is concentrated nowhere, and a radical concentrated nowhere cannot attack a neighbour.
So phenols do this job, and they do it for the plant first. Thyme and oregano build thymol and carvacrol — carvacrol leading in oregano, thymol leading in thyme — and clove builds eugenol at 70 to 90 per cent of its oil. One function these serve the plant is protecting its own volatile material from oxidising under strong sun. The same chemistry slows an oil going off in a bottle, and is what a laboratory assay measures.
What is measured, and what is not
An antioxidant assay is run in a tube, or on cells in a dish, at concentrations its operator chose. It measures a chemical behaviour of the material, not what happens in a person: nothing has been swallowed, digested, absorbed or cleared, and concentrations in human blood are far below the assay’s. A high laboratory antioxidant value is a fact about the material in the tube.
Photograph to come
Two halves of the same apple side by side on a pale wooden board, photographed straight down in soft daylight, twenty minutes after cutting. The left half visibly browned across the cut face. The right half still pale, with a cut lemon resting beside it and a faint sheen of juice on the flesh. No text, no props beyond the lemon, no styling — the point is that one variable changed. The colour difference must be obvious at phone size.
ORAC stands for oxygen radical absorbance capacity, worth knowing precisely because it is quoted so freely. A fluorescent probe goes into a tube with a compound that generates peroxyl radicals at a steady rate; the radicals attack the probe, its glow fades, and an instrument records how fast. Add the sample and run it again: if the glow lasts longer, the sample absorbed some of the radicals. The result is reported against trolox, a water-soluble relative of vitamin E, per gram.
Every word of that describes a tube. One kind of radical, generated artificially. No mouth, no stomach, no bile, no intestinal wall, no liver, none of the absorption steps that decide whether a compound reaches a cell. A figure per gram also rewards being undiluted, which is why an essential oil produces a large one by construction.
This is not a fringe objection. The United States Department of Agriculture withdrew its own reference database of ORAC values for foods in 2012, on the grounds that the values were being used to make claims about health outcomes the assay cannot support. The measurement is honest. The inference usually drawn from it is not.
A chain running through a membrane is happening in fat. A radical in blood plasma is happening in water. Two rooms — and as vitamins showed, a molecule that dissolves in one does not reach the other.
Vitamin E is built for the fatty room. A tocopherol molecule is a long hydrocarbon tail with a ring system on the end carrying one hydroxyl. The tail buries itself among the membrane’s fatty acids while the ring and its hydroxyl sit at the boundary where membrane meets water. Its recognised role is protecting membrane fats from oxidation, and the structure is how.
Give that hydrogen to a peroxyl radical and the chain stops, but vitamin E is now a tocopheroxyl radical: stabilised across its ring, and spent. This is where vitamin C arrives. Ascorbic acid is thoroughly water-soluble, sits in the plasma on the other side of that boundary, close enough to hand a hydrogen across. Vitamin E is restored. Vitamin C becomes an ascorbyl radical, which the body’s own enzymes return using glutathione. Neither vitamin is the antioxidant. The cycle is.
Diagram to come
A cross-section of a cell membrane filling the lower two thirds of the frame: two facing rows of phospholipids with round heads and paired tails, the space above the upper row clearly tinted as water. One tocopherol molecule embedded in the upper leaflet, its long tail down among the fatty tails and its ring system with its –OH up at the boundary, so a reader can see it is anchored rather than floating. Inside the membrane, one fatty acid tail carrying a peroxyl radical with a visible dot. Arrow one: a hydrogen travelling from the tocopherol –OH to that radical, which is marked as neutralised. The tocopherol ring is then redrawn as a tocopheroxyl radical with its unpaired electron shown as a shaded cloud over the ring, still at the boundary. Arrow two, coming down from the water side: an ascorbate molecule handing a hydrogen to that ring, the ring restored to tocopherol, and a return arrow closing the loop back to arrow one. Arrow three: the ascorbate, now an ascorbyl radical, moving to a small rounded box in the water labelled as the body’s own enzymes with glutathione named inside, and a fourth arrow returning restored ascorbate to the water. Draw both big loops as genuine closed circuits — the figure fails if it reads as a one-way sequence.
One honest consequence, and it is chemistry rather than advice. A tocopheroxyl radical with nothing to regenerate it does not stay inert forever; given long enough it can take a hydrogen from a fatty acid itself — the chain restarting from the molecule meant to stop it. Among its partners that is a non-event. Isolated, with nothing to hand an electron back, the same molecule behaves differently. Which is why "which antioxidant is best" has the wrong shape.
None of that is the body’s main answer to a radical. Its main answer is enzymatic, and an enzyme differs from a dietary compound as a tool differs from a consumable. A dietary phenol works once: one molecule, one hydrogen, spent. An enzyme is catalytic — restored after every cycle, sitting where radicals are produced, and running at a speed no dietary molecule approaches. Published turnover figures for catalase reach millions of molecules a second.
Three of them do most of the work, and each is built around a metal. That is the join with minerals as ions: the metal is not a passenger but the part that moves the electron, switching between two charges as iron does. An enzyme without its partner is a well-folded protein that does nothing — the subject of enzymes and cofactors.
| Defence | What it handles | Partner it needs | Once, or reused |
|---|---|---|---|
| Superoxide dismutase | Superoxide, turned into hydrogen peroxide and oxygen | Copper with zinc in the cell fluid; manganese in the mitochondria | Reused — catalytic |
| Catalase | Hydrogen peroxide, turned into water and oxygen | Iron, held inside a haem group | Reused — catalytic |
| Glutathione peroxidase | Hydrogen peroxide, and peroxides already formed on fats | Selenium, built into the protein chain itself | Reused — catalytic |
| Vitamin E in a membrane | One lipid peroxyl radical | Vitamin C, to be restored | Once, then needs regenerating |
| A phenol from food or a bottle | One radical | None | Once |
Selenium is the sharpest case. It is built into glutathione peroxidase as selenocysteine — an amino acid in which selenium stands where sulphur normally stands, one row down the same column, which is why it does the same chemistry more readily. That is the mechanism underneath a plain statement like selenium serves the enzymes that maintain the body’s own antioxidant defences: without the mineral there is no working enzyme.
Superoxide dismutase does not destroy superoxide. It converts it into hydrogen peroxide, which is itself reactive — progress in name only, until you notice two things. Hydrogen peroxide is far less reactive, so the urgency drops; and unlike a radical it is stable enough to be moved, so the second step need not happen at the same spot. Catalase and glutathione peroxidase take it apart in the compartments built for it. The design is a relay. That same stability is what lets hydrogen peroxide double as a signal between cells.
The most reliable use of this chemistry is not about your body but about your materials. Oxidation is why an oil ages: oxygen above the liquid, light, warmth, and cheap hydrogens on the molecules inside. Keep bottles capped, cool and in dark glass, and give the coolest place to the ones carrying the most double bonds — the citrus oils among them. An oxidised oil is not merely faded. It is chemically different, and likelier to irritate skin than when fresh.
The phenols carry the same consequence for handling: a molecule that gives up its hydroxyl hydrogen easily reacts with whatever it lands on, and skin registers that as irritation. Oregano, thyme, cinnamon bark, cassia and clove need heavy dilution in a carrier oil before any topical use, never neat, and safety holds this app’s dilution guidance. Expressed citrus oils — lemon, lime, grapefruit, bergamot, wild orange — also need dilution, and after applying them to skin, avoid direct sunlight or any UV source for up to twelve hours. Internal use of any oil is only ever appropriate if the label on your own bottle says it is for internal use; labelling, and the range itself, differ from market to market.
In the kitchen the chemistry is visible in seconds. Lemon juice on a cut apple slows the browning because ascorbic acid gives up its hydrogens first. Vitamin E on a fish-oil softgel guards the oil inside the capsule, where a fatty acid with six double bonds offers five cheap hydrogens — a statement about the softgel on the shelf, not about anything in a person. And when a label hands you a number, you know what to ask of it: which radical, at what concentration, in a tube or in a person.
Keep oils away from eyes and inner ears, and out of reach of children. Dilute before topical use, and dilute the phenolic oils heavily. If you are pregnant, nursing, under medical care or taking medication, speak to your healthcare practitioner before use. Laboratory antioxidant measurements describe how a material behaves in a tube or on cells in a dish and are not statements about what happens in a person. Nothing here is intended to diagnose, treat, cure or prevent any disease.
Lesson 16 of 18 · Science