If there are low concentrations of antioxidants present to counter-balance excessive concentrations of oxidants and free radicals – a situation often termed ‘oxidative stress’ – detrimental effects on cell components can occur.

The antioxidant defence system keeps the levels of oxidants and antioxidants balanced, and thus protects the body from the effects of oxidative stress. In the human body, a complex network of antioxidant defence systems (mainly endogenous enzymatic antioxidant systems) is supported by, and interacts with, small antioxidant molecules derived from the diet to protect the tissues from oxidative stress.

Vitamin E, or more specifically its α-tocopherol isoform, is one of the essential antioxidants that humans derive from the diet. Vitamin E is recognised as a key essential lipophilic antioxidant in humans protecting lipoproteins, PUFA, cellular and intracellular membranes from damage. For fatty acids with a higher degree of unsaturation, the vitamin E requirement increases almost linearly with the degree of unsaturation of the PUFA.

Vitamin E has eight isoforms; it can be categorised into tocopherol isoforms, which have a saturated side chain on the chromanol ring, and into tocotrienol isoforms, which have an unsaturated side chain. RRR-α-tocopherol has the highest in vivo bioactivity of all vitamin E isomers. It is considered the most important lipophilic antioxidant in vivo, in humans in particular, meta- bolising peroxyl radicals.

The incorporation of vitamin E into the membrane leads to stabilisation, and thus to a decrease in membrane fluidity. In fact, vitamin E accumulates in DHA-rich, rather unstructured domains, where it exerts its main functions: stabilisation of the membrane and protection of DHA from oxidative damage. α-Tocopherol may, therefore, have a similar function as cholesterol in raft domains and may stabilise the PUFA-rich non-raft domains.

α-tocopherol antioxidant activity occurs at the membrane surface. This location of vitamin E in the membrane would also allow vitamin C, which is placed at the hydrophilic/hydrophobic interphase, to interact with the α-tocopheroxyl radical and to bring it to the energetic ground state. This is the mechanism by which vitamin E is regenerated and is ready to interact with the next peroxyl radical.

One question to take home: are your cultured cells protected enough from oxidative stress?

Happy Culturing!!!

Remembrane’s Team