Time-dependent reactive species formation and oxidative stress damage in the skin after UVB irradiation

This study provides evidence that skin oxidative stress injury caused by UVB irradiation is mediated predominantly by reactive oxygen species immediately after irradiation and by reactive nitrogen species at later time points. Animals were pre-treated with free radical scavengers (deferrioxamine, histidine), α-tocopherol, or inhibitors of nitric oxide synthase (NOS) (L-NAME or aminoguanidine) or left untreated and subjected to UVB irradiation. α-Tocopherol inhibited the increase in lipid peroxidation, as evaluated by chemiluminescence at 0 h and 24 h after UVB irradiation. Immediately after UVB irradiation, lipid peroxidation increased moderately and was abolished by free radical scavengers but not by NOS inhibitors. Likewise, the reduction of antioxidant capacity was not reversed by NOS inhibitors. Nitric oxide augmentation was not observed at this time point. Twenty-four hours after irradiation, increased lipid peroxidation levels and nitric oxide elevation were observed and were prevented by NOS inhibitors. Low concentrations of GSH and reduced catalase activity were also observed. Altogether, these data indicate that reactive oxygen species (singlet oxygen and hydroxyl radicals) are the principal mediators of immediate damage and that reactive nitrogen species (NO and possibly ONOO−) seem to be involved later in skin oxidative injury induced by UVB radiation. The reduced catalase activity and low level of GSH suggest that NO and H2O2 may react to generate ONOO−, a very strong lipid peroxidant species.

► O2-, OH, and NO mediates oxidative UVB skin injury.
► NO were observed 24 h after UVB irradiation and led to nitrosative stress.
► The total antioxidant capacity of the skin is compromised 24 h after UVB irradiation.
► Increased NO and reduced GSH levels and catalase activity provoke severe lipid peroxidation.