Protective role of nitric oxide-mediated inflammatory response against lipid peroxidation in ultraviolet B-irradiated skin

Abstract

Ultraviolet (UV) irradiation is known to induce serious oxidative damage in the skin via lipid peroxidation. Nitric oxide (NO) synthesized by keratinocytes, melanocytes and endothelial cells in response to proinflammatory cytokines and UV radiation, has been reported to prevent UV-induced apoptosis in the skin. We have examined the effects of NO on UVB-induced lipid peroxidation in murine skin in vivo. UVB induced a dose-dependent increase in lipid peroxidation of skin extracts in vitro; however, lipid peroxidation in the skin in vivo remained unaffected at irradiation doses of less than 1.0 J cm-2 and decreased significantly at doses over 1.5 J cm-2 (P < 0.01). Time-delayed inhibition of lipid peroxidation in the skin in vivo was observed after irradiation at 1.5 J cm-2. Administration of N G-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, enhanced lipid peroxidation (P < 0.05), while it suppressed the ear-swelling response (ESR), a biological marker of inflammation. By contrast, administration of sodium nitroprusside, an NO enhancer, suppressed lipid peroxidation (P < 0. 01), while it enhanced the ESR. Expression of inducible nitric oxide synthase (iNOS) was observed from 12 to 48 h postirradiation at doses of 0.4-1.6 J cm-2. The UVB-induced iNOS expression was markedly inhibited by L-NAME, suggesting that iNOS is a major enzyme in the production of NO. These results suggest that NO acts as a mediator of the inflammatory response in UVB-irradiated skin, and that lipid peroxidation is inversely regulated with the NO-mediated inflammatory response in vivo.

Skin damage and mitochondrial dysfunction after acute ultraviolet B irradiation: relationship with nitric oxide production

“…In this study, the decrease in skin lipid peroxidation, even in the presence of mitochondrial O 2 •− production, was related to an increased cytosolic iNOS expression. Together, all these facts could be associated with the NO‐mediated inflammatory response, inducing protective signaling pathways against lipid peroxidation in the skin of irradiated animals, as described by other authors (28).…”

Influence of ultraviolet radiation on selected physiological responses of earthworms

“…A. gracilis was shown to be the most sensitive of the three species used in this study, while P. corethrurus showed no marked response to UV. Hairless mice exposed to 3000·J·m -2 UV-B show skin erythema, but do not die (Lee et al, 2000), while Tubefix dies when the UV-B energy is 5 times greater (Soni and Joshi, 1997) than that which kills A. gracilis. A. gracilis thus has a higher sensitivity than these organisms.…”

“…In recent times, the generally accepted animal model for UV studies has been the hairless mouse (Van Weelden and Van der Leub, 1985), but these animals are expensive to purchase and handle, and the relevant effects occur very slowly (Lee et al, 2000). Normally, terrestrial animals have higher tolerance to UV-B than aquatic animals (Gies et al, 1995), as many protect themselves from UV-B by pigments or integuments, such as feathers, hair, a shell or scales.…”

Topical ‘Sydney’ Propolis Protects against UV-Radiation-Induced Inflammation, Lipid Peroxidation and Immune Suppression in Mouse Skin

“…The homogenates were centrifuged sequentially at 10,000 g for 10 min and 20,000 g for 20 min at 4°C (Sorvall RC5B refrigerated centrifuge), retaining the supernatant after removal of the solidified surface lipid layer. Lipid peroxidation was quantitated in duplicate samples as the degradation product, malondialdehyde (MDA), complexed with thiobarbituric acid, as described by Ohkawa et al [26], and modified by Lee et al [27]. The protein content of the skin homogenate supernatants was measured by the Lowry assay [28], and the result expressed as the average MDA (p M )/protein (mg).…”