Lipid oxidation damages keratinocytes

Can a skin treatment improve the water barrier yet slow recovery after friction and drying? This hypothesis asks whether treatment-lipid oxidation causes that gap in human skin organ culture, skin tissue kept outside the body. It compares the original formulation with an equal amount of a deuterated version of linoleic acid, a polyunsaturated lipid. Before challenge, tissues must match in lipid incorporation, lipid-layer organization, water loss, hydration, mechanics and CD1a activity, a lipid-presentation pathway. Fewer oxidation products and improved recovery would support oxidation as a leading contributor. Lower oxidation with unchanged recovery would favour immune regulation or interface integrity. Measures of oxidized lipids and recovery would distinguish them.