We often talk about “sun damage”.
But what does that actually mean?
Does sunlight somehow burn through collagen?
Does UV simply dry the skin out?
And what on Earth do antioxidants have to do with any of it?
To understand that, we need to zoom right down into the chemistry happening inside our skin.
Because one of the most important consequences of ultraviolet exposure is something called: oxidative stress.
And despite the rather alarming name, oxidation itself is completely normal biology.
First, meet oxygen
We need oxygen to live.
But oxygen is chemically interesting.
During normal cellular metabolism, small quantities of highly reactive oxygen-containing molecules are continually produced.
These are collectively called reactive oxygen species — ROS.
They include molecules such as superoxide, hydrogen peroxide and singlet oxygen. ROS are not simply waste products or villains.
At controlled concentrations they participate in normal cellular signalling, immune responses and adaptation.
The problem is balance (I think you have heard that from us before).
When ROS production exceeds the ability of cells to neutralise or manage them, we call that state oxidative stress.
And UV radiation can tip that balance.
UV is energy
When ultraviolet radiation reaches skin, molecules within our cells absorb some of that energy.
That energy can trigger chemical reactions that produce reactive oxygen species.
UVA is particularly relevant to oxidative chemistry because it penetrates relatively deeply into skin.
UVB, meanwhile, is particularly important for direct DNA damage and sunburn, although both UVA and UVB contribute to biological damage. WHO describes UVA as penetrating into deeper skin tissues, while most UVB is absorbed within the epidermis.
Research into photoageing shows that UV-induced ROS can interact with lipids, proteins and DNA and can activate signalling pathways involved in inflammation and tissue remodelling.
This is where “sun damage” suddenly becomes much more interesting than a wrinkle.
Think of ROS as chemical sparks
One useful analogy is sparks from a fire. A few sparks are manageable, and your skin has systems designed to deal with them. But if sparks are being created faster than they can be extinguished, they begin reacting with everything around them.
Cell membranes contain lipids. ROS can oxidise those lipids in a process called lipid peroxidation.
Proteins can also be oxidatively modified.
DNA can be damaged.
And because some oxidation products are themselves reactive, one reaction can trigger others - like a cascading effect.
It is chemistry with momentum.
Collagen isn't simply “destroyed by the sun”
There is another layer to the story.
ROS don't only damage molecules directly. They also act as biological signals.
UV-induced oxidative stress can activate cellular signalling pathways including MAPK, AP-1 and NF-κB. These pathways influence inflammation and can increase expression of enzymes called matrix metalloproteinases — MMPs.
MMPs are perfectly normal enzymes involved in tissue remodelling.
But increased MMP activity following repeated UV exposure can contribute to breakdown and disorganisation of extracellular-matrix components, including collagen.
At the same time, UV exposure can alter collagen production.
Repeated over years, this contributes to the structural changes we recognise as photoageing.
So the story isn't:
UV hits collagen and collagen disappears.
It is an interconnected biological response involving oxidative chemistry, cellular signalling, inflammation, enzymes, repair and repeated exposure.
Much more interesting.
And pollution can enter the same chemistry
UV isn't the only environmental trigger.
Airborne particulate matter can also promote ROS formation in skin.
Research has found that particulate pollution can contribute to lipid peroxidation, protein modification, inflammatory signalling and barrier dysfunction.
One particularly interesting target is squalene.
Squalene is a lipid naturally present in human sebum.
Because it contains multiple carbon-carbon double bonds, it is particularly susceptible to oxidation.
Pollution-associated oxidative chemistry can therefore alter the composition of the very oils coating the surface of our skin.
That is a rather remarkable thought.
The outside environment can change the chemistry of the skin surface before anything has even penetrated deeply into the tissue.
But oxidation does not mean your skin is helpless
Quite the opposite.
Skin comes equipped with an impressive antioxidant network.
- Superoxide dismutase.
- Catalase.
- Glutathione.
- Glutathione peroxidase.
- Vitamin C.
- Vitamin E.
- Coenzyme Q10.
- Uric acid.
And many other interacting molecules and enzymes. Their job is not to eliminate every reactive oxygen molecule. That would actually interfere with normal biology.
Their job is to maintain redox balance.
Think less:
ROS = bad. Antioxidants = good.
And more:
healthy skin is managing a chemistry in balance.
So where does skincare fit?
First — and most importantly — reducing excessive UV exposure makes far more sense than trying to repair unlimited exposure afterwards.
Sunscreen, shade, clothing and sensible sun behaviour remain primary protection.
An antioxidant serum is not permission to sunbathe. Neither is eating blueberries.
But once we understand oxidative stress, we can also understand why researchers are interested in antioxidant molecules, barrier-supportive compounds and compounds that influence inflammatory or oxidative signalling.
The aim is not to stop normal oxidation.
It is to support the skin in maintaining equilibrium.
And that brings us to an even more interesting question:
If oxidative stress is happening in skin every day, what defence systems has the skin evolved to manage it?
Quite a few, as it turns out.