Abstract
Occlusion of the skin with a water-vapor-impermeable membrane following disruption of the permeability barrier prevents the epidermal changes which lead to the restoration of barrier function, suggesting that water transit could be an important regulatory signal for barrier repair. However, occlusion with a water-vapor-impermeable membrane also prevents the movement of gases, which could also potentially influence permeability barrier homeostasis. Since O2 is known to have an effect on epidermal cell function, we have determined the effect of gases containing different levels of O2 on barrier repair 6 h following topical treatment of hairless mice with acetone. The disrupted barrier of air-exposed animals (O2 ∼ 20%) recovered by 50.8 ± 3.4% (mean ± SEM) after 6 h. Under flowing air (O2 ∼ 20%), O2/CO2 95/5 % and argon (O2 = 0%) the barrier recovered by 43.9 ± 28, 36.2 ± 8.5 and 39.2 ± 4.6%, respectively. These values were not statistically different from each other. The slightly lower levels of recovery at 6 h with the flowing gases in comparison to exposure to static air probably can be attributed to a slight cooling of the skin caused by the flowing gases. These results suggest that exogenous O2 is neither required for barrier repair nor a signal for barrier repair.