Oxidative stress and your antioxidant genes

Oxidative stress is the slow background damage behind much of ageing and chronic disease. Everyone makes free radicals; the difference is how efficiently you mop them up.

Free radicals are a fact of metabolism

Turning food and oxygen into energy unavoidably generates reactive oxygen species. In balance they are managed; in excess they damage lipids, proteins and DNA, contributing to ageing and disease. Your antioxidant defence keeps the balance.

Your antioxidant relay

The defence works as a relay of enzymes. SOD2 converts mitochondrial superoxide into hydrogen peroxide; GPX1 (selenium-dependent) and CAT then break that hydrogen peroxide down to water; and NQO1 regenerates other antioxidants such as Coenzyme Q10. A weak link anywhere lets damage through.

Where the weak links appear

Common variants reduce the efficiency of these enzymes, so two people with the same diet can have very different antioxidant reserves. Knowing where your chain is weakest tells you which antioxidants are worth prioritising rather than guessing.

What actually helps

The most effective support is a network: vitamins C and E as front-line antioxidants, selenium for GPX1, the cofactors zinc and manganese (manganese feeds SOD2), and alpha-lipoic acid to regenerate the others. The right mix depends on your genotype.

The science, in depth

SOD2 (MnSOD) dismutes superoxide to H₂O₂, which GPX1 and catalase reduce to water; NQO1 performs two-electron quinone reduction that recycles ubiquinol and other antioxidants. Functional polymorphisms across SOD2, GPX1, CAT and NQO1 grade enzyme efficiency, so individual antioxidant requirements vary with the combined genotype.