UVB-induced Lipid Peroxidation Research Articles

Differences in rutin effect on membrane phospholipids in skin fibroblasts irradiated with UVA and UVB

Chronic exposure of the skin to solar UV radiation induces a number of biological alterations, including a redox imbalance; therefore, there is a constant need for protective compounds, particularly natural antioxidants. The aim of this study was to determine the effect of rutin on interactions between membrane phospholipid and antioxidant proteins expression in UVA or UVB irradiated fibroblasts. Following exposure to UVA and UVB irradiation cells were incubated with rutin 12h before and/or up to 24h after irradiation, and the structural and metabolic changes were examined at selected time intervals. Rutin penetration through the fibroblast phospholipid bilayer was aided by UVA-induced bilitranslocase activity, while lipidomic analysis revealed that following UVB-irradiation rutin transport into cell is enhanced by changes in membrane permeability resulting from UVB-induced lipid peroxidation. Moreover, rutin partially prevented UVA/B-induced increase in phosphatidylethanolamine and phosphatidylcholine and decrease in sphingomyelin, as well as their membrane localization. However, the inhibition of phospholipase A2 activity and increase in ROS level resulted in protection against the reduction of phospholipids/free arachidonic and linoleic acids and the increase in the level of the lipid peroxidation product 4-HNE, which demonstrates the antioxidant proteins regulatory properties. The antioxidant activity of rutin, effectively prevented the enhanced ROS generation as well as antioxidant system destruction. Proteome analysis show that rutin treatment more strongly protects against UVA-induced rather than UVB-induced increases in the total expression of proteins involved in antioxidant response (such as SOD, TrxR, and Prxs 1/2). However, in the case of UVB-irradiated cells, rutin additionally enhances the levels of disulfide-isomerase – an enzyme that is responsible for the formation and breakage of disulfide bonds, what in the case of Nrf2/ARE pathway has significant meaning in the Nrf2 transcriptional activity level and leads to the synthesis of cytoprotective proteins. In conclusion, UVA and UVB radiation in partially different ways affect rutin interactions with the fibroblast biomembrane lipids as well as antioxidant proteins. Rutin membrane penetration is promoted by UVA-induced bilitranslocase activity, while UVB irradiation enhanced membrane permeability to facilitate the interaction of rutin with phospholipids. Moreover, rutin particularly influences UVA-induced antioxidant proteins expression and UVB-induced transcription signaling.

Nanoencapsulation of Cyanidin-3- O-glucoside Enhances Protection Against UVB-Induced Epidermal Damage through Regulation of p53-Mediated Apoptosis in Mice.

Excess ultraviolet (UV) radiation causes numerous forms of skin damage. The aim of the present study was to assess and compare the photoprotective effects of cyanidin-3- O-glucoside (C3G) alone and encapsulated in chitosan nanoparticles (Nano-C3G) in a UVB-induced acute photodamage mouse model. Nano-C3G was developed from chitosan and sodium tripolyphosphate (TPP) by ionic gelation. The particle size, zeta potential, entrapment efficiency, drug loading, and in vitro release in 6 days were determined. Kunming (KM) mice were treated with Nano-C3G (125, 250, 500 μM) or C3G (500 μM) after part of the dorsal skin area was dehaired and then exposed to 2 J/cm2 of UVB. The nanocapsules were successfully produced and had a uniform and complete spherical shape without agglomeration. The size, zeta potential, entrapment efficiency, and drug loading of Nano-C3G was 288 nm, +30 mV, 44.90%, and 4.30%, respectively. C3G in the nanocapsules was released quite rapidly, and the release rate slowed down at higher pH. The animal experiment demonstrated that Nano-C3G could effectively reduce the UVB-induced lipid peroxidation, malondialdehyde, and 8-hydroxy-2'-deoxyguanosine contents; downregulate p53, Bcl-2-associated X (Bax), and caspase-3 and -9 expression; and balance the B-cell lymphoma-2/leukemia-2 ratio. Moreover, Nano-C3G (125, 250, 500 μM) improved the visual appearance, skin moisture, histologic appearance, and apoptotic index (based on TUNEL staining) under UVB exposure. In conclusion, these results suggest that Nano-C3G can reduce UVB-induced epidermal damage through the p53-mediated apoptosis signaling pathway. Moreover, Nano-C3G was more efficient than C3G at the same concentration (500 μM).

The Antioxidant Activity of Peptides Isolated from Amaranthus on Normal Human Skin in vitro and Inflammatory Cytokines Detection

Oxidative stress has been implicated in various skin diseases through the generation of reactive oxygen species and the depletion of endogenous antioxidant systems. Evidence exists indicating that oxidative stress injury of the skin caused by UVB irradiation is mediated predominantly by reactive oxygen species (ROS) immediately after irradiation and by reactive nitrogen species (RNS) at later points. We investigated the protective effect of peptides (albumin and hydrolysates) isolated from Amaranthus (pA) against UVB irradiation, lipid peroxidation (malondialdehyde, MDA) and endogenous antioxidant defense enzymes such as glutathione peroxidase (GPX), superoxide dismutase (SOD) and catalase (CAT). Supernatant levels of pro-inflammatory and anti-inflammatory cytokines were also investigated. We used human skin organ culture as an in vitro model via 24, 36 and 48 hrs of culture. The pA has a significant protective effect via the inhibition of damaged caused by UVB irradiation. The treatment of skin with pA inhibited the UVB-induced lipid peroxidation. Additionally, this pA-inhibited UVB-induced depletion of antioxidant defense components, such as, CAT, SOD, and GPX, and the final antioxidant treatment also reduced levels of pro-inflammatory cytokines: IL-1beta, IL-12, TNF and INF-gamma. We conclude that pA could be useful in attenuating UVB-induced oxidative stress and mitigating skin diseases in human skin due to antioxidant properties.

Coptis chinensis inflorescence extract protection against ultraviolet-B-induced phototoxicity, and HPLC–MS analysis of its chemical composition

Cultivated Coptis chinensis inflorescence has been highly valued in Chinese tea production for many years. The main alkaloid compounds in C. chinensis inflorescence ethanolic extracts (CE) were identified by high-performance liquid chromatography–mass spectrometry. The detected compounds included jatrorrhizine (4.87mg/g), coptisine (17.18mg/g), palmatine (3.32mg/g), and berberine (31.81mg/g), as well as columbamine and epiberberine (tentatively identified). CE protective activity against ultraviolet-B (UVB)-induced phototoxicity in a mitochondria model was determined by measuring thiobarbituric acid-reactive substrates, lipid hydroperoxide, conjugated diene, 4-hydroxynonenal, and glutathione. The results showed that CE excellently inhibited UVB-induced lipid peroxidation and glutathione reduction in vitro. This photoprotective effect of CE may be caused by the presence of the abovementioned alkaloid compounds and phenolic compounds that enhances CE antioxidant activity. Therefore, CE possesses potent photoprotective property that may find valuable applications in food industries and in anti-phototoxicity formulations.

Photoprotective Effects of Two Natural Products on Ultraviolet B–Induced Oxidative Stress and Apoptosis in SKH-1 Mouse Skin

Solar ultraviolet radiation (UV) is the major cause of nonmelanoma skin cancer in humans. Photochemoprevention with natural products represents a simple but very effective strategy for the management of cutaneous neoplasia. We studied the photoprotective activity of Calluna vulgaris and red grape seed (Vitis vinifera L, Burgund Mare variety [BM]) extracts in vivo in an SKH-1 hairless mice skin model. Fifty 8-week-old female SKH-1 hairless mice were randomly divided into 5 groups (n = 10 each): controls, UVB-irradiated, C. vulgaris plus UVB-irradiated, BM plus UVB-irradiated, and epigallocatechin gallate (EGCG) plus UVB-irradiated. A dose of 4 mg/mouse per cm² of skin area for both extracts was topically applied to the mice 30 minutes before a single-dose (240 mJ/cm²) UVB exposure. EGCG dissolved in phosphate-buffered saline (pH 6.6; 0.067 M) was administered at 2 mg/mouse per cm². Glutathione peroxidase and catalase activities, reduced glutathione (GSH), malondialdehyde, nitric oxide, and caspase 3 activity were determined in skin homogenates 24 hours after irradiation. A single dose of UVB increased GSH levels and glutathione peroxidase activity in the exposed skin. C. vulgaris and BM pretreatment significantly decreased GSH formation and glutathione peroxidase activity (P < .001) and inhibited UVB-induced lipid peroxidation (P < .0001) and nitric oxide production (C. vulgaris: P < .06). Topical treatments with C. vulgaris and particularly BM extracts (P < .002) significantly reduced caspase 3 activity, indicating that the cells were protected against apoptosis. These results suggest that C. vulgaris and BM extracts might be chemopreventive candidates for reducing UV-induced risk for skin cancer.

Protective Effect of Carvacrol on Oxidative Stress and Cellular DNA Damage Induced by UVB Irradiation in Human Peripheral Lymphocytes.

Exposure to ultraviolet B (UVB; 280-320 nm) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of carvacrol on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular an-tioxidant status in human lymphocytes. A series of in vitro assays (hydroxyl radical, superoxide, nitric oxide, DPPH (2,2-Diphenyl-1-picryl hydrazyl), and ABTS (2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging assays) demonstrate antioxidant property of carvacrol in our study. UVB exposure significantly increased thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LHPs), % tail DNA and tail moment; decreased % cell viability and antioxidant status in UVB-irradiated lymphocytes. Treatment with carvacrol 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA, and tail moment and increased % cell viability as carvacrol concentration increased. UVB irradiated lymphocytes with carvacrol alone (at 10 μg/mL) gave no significant change in cell viability, TBARS, LHP, % tail DNA, and tail moment when compared with normal lymphocytes. On the basis of our results, we conclude that carvacrol, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced ROS.

Effect of ursolic acid, a triterpenoid antioxidant, on ultraviolet-B radiation-induced cytotoxicity, lipid peroxidation and DNA damage in human lymphocytes

Exposure to ultraviolet B (UVB, 280–320) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of ursolic acid on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular antioxidant status in human lymphocytes. Series of in vitro tests (hydroxyl radical, superoxide, nitric oxide, DPPH and ABTS radical scavenging assays) demonstrates antioxidant property of ursolic acid in our study. Treatment of lymphocytes with ursolic acid alone (at 10 μg/mL) gave no significant change in cell viability, thiobarbituric acid reactive substances (TBARSs), lipid hydroperoxides (LHPs), % tail DNA and tail moment when compared with normal lymphocytes. UVB-exposure significantly increased TBARS, LHP and % tail DNA, tail moment; decreased % cell viability and antioxidant status in irradiated lymphocytes. Treatment with ursolic acid 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA and tail moment and increased % cell viability as ursolic acid concentration increased. Based on our results we conclude that ursolic acid, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced reactive oxygen species.

Ferulic acid inhibits UV-B–induced oxidative stress in human lymphocytes

UV-B induces lipid peroxidation and oxidative stress in mammalian cells by producing reactive oxygen species. In this present study, we report the protective effect of ferulic acid (FA; 3-methoxy-4-hydroxycinnamic acid), a dietary antioxidant, on UV-B–induced oxidative stress and lipid peroxidation using normal human lymphocytes. Treatment of the human peripheral lymphocytes with UV-B irradiation caused a significant (P b .05) depletion of reduced glutathione (GSH) levels, superoxide dismutase, catalase, and GSH peroxidase activities, and increased the levels of thiobarbituric acid–reactive substances. Treatment of human lymphocytes with FA before 30 minutes of irradiation inhibited UV-B–induced lipid peroxidation. Ferulic acid also inhibited UV-B–induced depletion of antioxidant defense components, such as GSH peroxidase, catalase, superoxide dismutase, and GSH. The maximum dose of FA (10 μg/mL) normalized the UV-B–induced oxidative stress, indicating the protective effect of FA in human peripheral lymphocytes under in vitro conditions against UV-B exposure. Our observations suggest that FA reduces UV-B–induced lipid peroxidation and enhances antioxidant status in human lymphocytes exposed to UV-B radiation, and therefore, FA could serve as a protector against the UV-B–induced pathologic changes. © 2007 Elsevier Inc. All rights reserved.

Divergent Optimum Levels of Lycopene, β-Carotene and Lutein Protecting Against UVB Irradiation in Human Fibroblasts¶

Exposure of living organisms to UV light leads to photooxidative reactions. Peroxyl radicals are involved in the propagation of lipid peroxidation. Carotenoids are dietary antioxidants and show photoprotective effects in human skin, efficiently scavenging peroxyl radicals and inhibiting lipid peroxidation. Cultured human skin fibroblasts were used to examine the protective effects of the carotenoids, lycopene, β-carotene and lutein on UVB-induced lipid peroxidation. The carotenoids were delivered to the cells using liposomes as the vehicle. The cells were exposed to UVB light for 20 min. Lycopene, β-carotene and lutein were capable of decreasing UV-induced formation of thiobarbituric acid-reactive substances at 1 h to levels 40–50% of controls free of carotenoids. The amounts of carotenoid needed for optimal protection were divergent at 0.05, 0.40 and 0.30 nmol/mg protein for lycopene, β-carotene and lutein, respectively. Beyond the optimum levels, further increases of carotenoid levels in cells led to prooxidant effects.

Topically Applied Eicosapentaenoic Acid Protects Against Local Immunosuppression Induced by UVB Irradiation, cis-Urocanic Acid and Thymidine Dinucleotides¶

UVB-induced immunosuppression, a promoter of photocarcinogenesis, involves the formation of pyrimidine dimers and cis-urocanic acid (cis-UCA), but reactive oxygen species (ROS) also plays an important role. Eicosapentaenoic acid (EPA) can inhibit photocarcinogenesis, but due to its polyunsaturated nature it is susceptible to oxidative damage by ROS. The antioxidant defense system may therefore be challenged upon ultraviolet-B (UVB) irradiation in the presence of EPA. We investigated whether topically applied EPA in mice could protect against local immunosuppression (contact hypersensitivity response to dinitrofluorobenzene) induced by UVB radiation (1.5 J/cm2), or topically applied cis-UCA (150 nmol/cm2) or thymidine dinucleotides (pTpT) (5 nmol/cm2). The influence of EPA on epidermal lipid peroxidation and antioxidant status was also measured. UVB irradiation, cis-UCA and pTpT all caused 70% immunosuppression. Topical pretreatment of mice with EPA partially protected against immunosuppression; the EPA dose needed to accomplish this was 10 nmol/cm2 for UVB irradiation, 100 nmol/cm2 for cis-UCA and 1000 nmol/cm2 for pTpT. Higher EPA doses caused higher UVB-induced lipid peroxidation and lower vitamin C levels. Glutathione only decreased with the highest EPA dose whereas vitamin E was not decreased after UVB irradiation. In conclusion, topically applied EPA protects against UVB-, cis-UCA- and pTpT-induced immunosuppression and maintenance of an adequate antioxidant defense seems to be an important prerequisite for the protective action by EPA.

A New Wrinkle on Topical Vitamin E and Photo-inflammation: Mechanistic Studies of a Hydrophilic γ-Tocopherol Derivative Compared with α-Tocopherol

The antioxidant function of vitamin E is thought to mediate its photo-protective effects. Cyclooxygenase-2 (COX-2) is an important mediator of early photo-inflammation. Thus, the ability of gamma-tocopherol to inhibit COX-2 activity independently of its antioxidant function raises important questions regarding potential roles that this form of vitamin E plays in photo-protection and skin cancer chemoprevention.

Xanthophylls and α-Tocopherol Decrease UVB-Induced Lipid Peroxidation and Stress Signaling in Human Lens Epithelial Cells

Epidemiological studies suggest that consumption of vegetables rich in the xanthophylls lutein (LUT) and zeaxanthin (ZEA) reduces the risk for developing age-related cataract, a leading cause of vision loss. Although LUT and ZEA are the only dietary carotenoids present in the lens, direct evidence for their photoprotective effect in this organ is not available. The present study examined the effects of xanthophylls and alpha-tocopherol (alpha-TC) on lipid peroxidation and the mitogen-activated stress signaling pathways in human lens epithelial (HLE) cells following ultraviolet B light (UVB) irradiation. When presented with LUT, ZEA, astaxanthin (AST), and alpha-TC as methyl-beta-cyclodextrin complexes, HLE cells accumulated the lipophiles in a concentration- and time-dependent manner with uptake of LUT exceeding that of ZEA and AST. Pretreatment of cultures with either 2 micromol/L xanthophyll or 10 micromol/L alpha-TC for 4 h before exposure to 300 J/m(2) UVB radiation decreased lipid peroxidation by 47-57% compared with UVB-treated control HLE cells. Pretreatment with the xanthophylls and alpha-TC also inhibited UVB-induced activation of c-JUN NH(2)-terminal kinase (JNK) and p38 by 50-60 and 25-32%, respectively. There was substantial inhibition of UVB-induced JNK and p38 activation for cells containing <0.20 and approximately 0.30 nmol xanthophylls/mg, respectively, whereas >2.3 nmol alpha-TC/mg protein was required to significantly decrease UVB-induced stress signaling. These data suggest that xanthophylls are more potent than alpha-TC for protecting human lens epithelial cells against UVB insult.

Photoprotective effect of sesamol on UVB-radiation induced oxidative stress in human blood lymphocytes in vitro

Normal lymphocytes are highly sensitive to the damaging effect of radiation and undergo cell death. In the present study, the photoprotective effect of sesamol, a constituent of sesame oil, has been examined in the UVB-(280–320 nm) irradiated human blood lymphocytes. Lymphocytes pretreated with increasing concentrations of sesamol (1, 5 and 10 μg/ml) for 30 min, were irradiated and lipid peroxidation and antioxidant defense were examined. UVB-irradiated lymphocytes exhibited increased levels of lipid peroxidation and disturbances in antioxidant defense. Sesamol pretreatment resulted in significant reduction in lipid peroxidation marker, thiobarbituric acid reactive substances (TBARS). Further, antioxidants like reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) increased, in a dose-dependent manner, in sesamol pretreated and UVB-irradiated lymphocytes. The maximum dose of sesamol (10 μg/ml) normalized the UVB induced lipid peroxidation, indicating the photoprotective effect of sesamol in irradiated lymphocytes.

Antioxidant protection in cultured corneal cells and whole corneas submitted to UV-B exposure

Several corneal pathologies are characterized by the presence of reactive oxygen species (ROS); therefore, we evaluated the protection afforded by pirenoxine and melatonin to corneal cell culture and whole rabbit cornea from ultraviolet exposure and other oxidant systems. Rabbit cornea cell (SIRC) plates and whole corneas were exposed to UV-B (80 or 800 mJ/cm 2) or incubated with fMLP-stimulated autologous macrophages, in the presence or absence of pirenoxine or melatonin (10 −5 M). The protective activity of compounds was assessed by measuring superoxide anion formation, inhibition of oxidation and mitochondrial viability. Moreover the ex vivo protective effect of pirenoxine and melatonin was verified in the whole cornea submitted to UV-B exposure in vitro. Our experimental data demonstrate that pirenoxine and melatonin were able to inhibit the superoxide formation and oxidative effect in cell culture and whole rabbit corneas submitted to UV-B exposure or to incubation with fMLP-stimulated autologous macrophages. Mitochondrial viability was restored in epithelial cells of rabbit cornea but not in SIRCs. Moreover, both compounds are also able to increase ex vivo epithelial corneal cell defences against the in vitro UV-B induced lipid peroxidation.

Divergent optimum levels of lycopene, beta-carotene and lutein protecting against UVB irradiation in human fibroblastst.

Exposure of living organisms to UV light leads to photooxidative reactions. Peroxyl radicals are involved in the propagation of lipid peroxidation. Carotenoids are dietary antioxidants and show photoprotective effects in human skin, efficiently scavenging peroxyl radicals and inhibiting lipid peroxidation. Cultured human skin fibroblasts were used to examine the protective effects of the carotenoids, lycopene, beta-carotene and lutein on UVB-induced lipid peroxidation. The carotenoids were delivered to the cells using liposomes as the vehicle. The cells were exposed to UVB light for 20 min. Lycopene, beta-carotene and lutein were capable of decreasing UV-induced formation of thiobarbituric acid-reactive substances at 1 h to levels 40-50% of controls free of carotenoids. The amounts of carotenoid needed for optimal protection were divergent at 0.05, 0.40 and 0.30 nmol/mg protein for lycopene, beta-carotene and lutein, respectively. Beyond the optimum levels, further increases of carotenoid levels in cells led to prooxidant effects.

Topically applied eicosapentaenoic acid protects against local immunosuppression induced by UVB irradiation, cis-urocanic acid and thymidine dinucleotides.

UVB-induced immunosuppression, a promoter of photocarcinogenesis, involves the formation of pyrimidine dimers and cis-urocanic acid (cis-UCA), but reactive oxygen species (ROS) also plays an important role. Eicosapentaenoic acid (EPA) can inhibit photocarcinogenesis, but due to its polyunsaturated nature it is susceptible to oxidative damage by ROS. The antioxidant defense system may therefore be challenged upon ultraviolet-B (UVB) irradiation in the presence of EPA. We investigated whether topically applied EPA in mice could protect against local immunosuppression (contact hypersensitivity response to dinitrofluorobenzene) induced by UVB radiation (1.5 J/cm2), or topically applied cis-UCA (150 nmol/cm2) or thymidine dinucleotides (pTpT) (5 nmol/cm2). The influence of EPA on epidermal lipid peroxidation and antioxidant status was also measured. UVB irradiation, cis-UCA and pTpT all caused 70% immunosuppression. Topical pretreatment of mice with EPA partially protected against immunosuppression; the EPA dose needed to accomplish this was 10 nmol/cm2 for UVB irradiation, 100 nmol/cm2 for cis-UCA and 1000 nmol/cm2 for pTpT. Higher EPA doses caused higher UVB-induced lipid peroxidation and lower vitamin C levels. Glutathione only decreased with the highest EPA dose whereas vitamin E was not decreased after UVB irradiation. In conclusion, topically applied EPA protects against UVB-, cis-UCA- and pTpT-induced immunosuppression and maintenance of an adequate antioxidant defense seems to be an important prerequisite for the protective action by EPA.

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

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.

Postadministration Protective Effect of Magnesium‐L‐ascorbyl‐phosphate on the Development of UVB‐induced Cutaneous Damage in Mice

The effects of stable vitamin C, magnesium-L-ascorbyl-2-phosphate (MAP), administered after acute and chronic exposure to UVB irradiation were investigated using hairless mice. Intraperitoneal administration of 100 mg/kg of MAP immediately after acute exposure to 15 kJ/m2 of UVB significantly prevented increases of UVB-induced lipid peroxidation in skin and sialic acid in serum, an inflammation marker. Administration of 50 mg/kg of MAP immediately after each exposure significantly delayed skin tumor formation and hyperplasia induced by chronic exposure to 2 kJ/m2 of UVB. Intraperitoneal administration of 200 mg/kg of MAP produced an increase in ascorbic acid (As) levels in the serum, liver and skin within 15 min. Serum As levels quickly returned to normal, but hepatic and cutaneous levels remained elevated before returning to normal after 24 h, suggesting that MAP was converted to As in the serum and in those tissues. Ultraviolet B-induced hydroxyl radical generation in murine skin homogenates was scavenged by As-Na addition, which was directly detected by electron spin resonance (ESR). These results suggest that postadministration of MAP delays progression of skin damage induced by UVB irradiation. It is presumed that MAP, once converted to As, exhibits such inhibitory effects by scavenging hydroxyl and lipid radicals generated as a direct or indirect result of UVB exposure.

Antioxidant effect of inorganic ions on UVC and UVB induced lipid peroxidation

Phosphate buffer suspensions of unilamellar liposomes of phosphatidylcholine were irradiated with UVC (254 nm) and UVB (300 nm) light. The irradiation provoked lipid peroxidation and liposome lysis with release of entrapped glucose-6-phosphate. At the same intensity of absorbed light, the photochemical effect at 254 nm is higher than at 300 nm. The addition of copper(II) and manganese(II) reduced both the peroxidation and the lysis. The copper showed an inhibitory effect only on the process provoked by the 254 nm irradiation, whereas the manganese was efficient both at 254 and 300 nm. The results are interpreted with a mechanism of peroxidation and quenching, involving photoformation of peroxyl radicals that are scavenged by manganese(II) and copper(I), with consequent breaking of the radical chain and reduction of the peroxidation rate. The copper(I), which is the active species, can be formed only at 254 nm by electron capture. The experimental data fit the kinetic equations obtained by the proposed mechanism by means of computer software.