Living in the city can be stressful to the skin: high concentrations of pollutants in the air will stress your skin through the production of free radicals. Free radicals are high energy molecules that are missing an electron and will go about starting chain reactions and destroying molecules in their search for the missing electron. The molecules they stole electrons from will become ROS* themselves and continue a chain reaction.
What we see in a polluted city is a “cloud” of very fine particles floating in the air, and the air smells strange. We should be concerned because those fine particles are full of strong oxidants that can increase respiratory and cardiovascular disease.
Our skin deals with reactive oxygen species (ROS*) all the time, because our own body makes them, byproducts of respiration by mitochondria. We have sophisticated mechanisms to deal with them that include multiple enzymes, proteins and low molecular antioxidants. The problem arises when we are bombarded with so much ROS* that the natural mechanisms we have to deal with them get overloaded.
When UV radiation reaches our skin, and when pollutants in the air that surrounds exceed by several orders of magnitude what exists in clean air. In the unspoiled Amazon you may find 1 μg per m-3 of fine particulate matter (and the ROS* that comes with it) , while in a polluted city there may be one thousand times as much.
What happens when all of those ROS*, whatever their composition reach our skin? Our skin suffers oxidative stress.
Proteins, lipids, DNA, and more cellular components will also be damaged, not just the cells but also the extracellular matrix, which is vital to our skin physiology and appearance.
DNA damage is the basis of UV-induced skin carcinogenesis, and ROS* are responsible in part for the damage done by UV. Mutated cells will also result in variations in skin pigmentation, either hyperpigmentation (sun or age spots) or hypopigmentation.
Protein changes are reflected in the skin by a decrease in total amount of proteins, and alterations of the structure of proteins that are crucial to skin function, like collagen and elastin. Protein can be oxidized in many ways, resulting in carbonylation, oxidation of sulfated amino acids and breaks in the amino acid chain. The fine structure of skin proteins will be distorted and broken proteins will be messed up and the organized fiber structure will collapse.
Oxidation of hyaluronic acid will result in breaks and decreased viscosity.
Mitochondrial damage by ROS* leads to decreased energy production and even cell death.
In short, if your skin’s antioxidant system is overwhelmed, the consequences will show as wrinkles, irregular pigmentation, loss of elasticity and what we know as aged skin. Most of the damage we see in aged skin has been caused by ROS* and not by intrinsic aging.
Should you worry about ROS* and oxidative stress? If you live in a polluted city, or if you smoke, or spend a lot of time in traffic, or if you go out in the sun without sunscreen – the answer is yes. What can you do? First of all, always wear sunscreen. But, what to do about pollution?
Thick silicone creams will not fix the problem. Pollution will bypass this “barrier” plus your skin will suffer if you cover it with a thick layer of silicones.
What you can do is supplement, “top-up” your own antioxidant system. Antioxidants act as a cooperative network and work well. So look at your skin antioxidant system and add more of what is already there.
Your skin antioxidant system includes small antioxidant molecules (ascorbic acid, glutathione, tocopherols (vitamin E), plus enzymes and proteins that regenerate the reduced forms of antioxidants, and disarm ROS* (superoxide dismutase or SOD, peroxidases and catalases). There are also enzymes capable of repairing some oxidized amino acids and proteins (MSRs).
Skin Actives ROS BioNet was designed to prevent oxidative stress and the damage it can do to your skin. Layer this light cream under sunscreen to fight oxidative stress; it makes a perfect addition to any daytime routine
Harman, D. (1983). Free radical theory of aging: consequences of mitochondrial aging. Age 6:86–94.
Hampton, T. (2005) Study reveals mitochondrial role in aging. JAMA, 294:672.
Liu, J., Atamna, H Kuratsune, H., Ames, BN. (2002) Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites Ann N Y Acad Sci, 959: 133-66
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