Assessment of the skin photoprotective capacities of an organo-mineral broad-spectrum sunblock on two ex vivo skin models.

UV irradiation can cause cutaneous damage that may be specific according to the wavelength of UV rays. For example, damage from UVB irradiation manifests itself in the form of sunburn cells and enhancement of the expression of p53, while damage from UVA exposure results in an increase in the expression of vimentin. These reactions to UV irradiation were used in this work to evaluate the photoprotective capacities of two sunblock preparations that were applied to the surface of the skin.

Photosensitization of DNA damage by a new cationic pyropheophorbide derivative: sequence-specific formation of a frank scission.

Pyropheophorbides are red-absorbing porphyrin-like photosensitizers that may interact with DNA either by intercalation or by external binding with self-stacking according to the value of the nucleotide to chromophore molar ratio (N/C). This article reports on the nature and sequence selectivity of the DNA damage photoinduced by a water-soluble chlorhydrate of aminopyropheophorbide. First, this pyropheophorbide is shown to induce on irradiation the cleavage of phiX174 DNA by both Type-I and -II mechanisms, suggested by scavengers and D2O effects.

Modifications of in vitro skin penetration under solar irradiation: evaluation on flow-through diffusion cells.

The effect of solar irradiation on ex vivo dermatomed hairless rat skin samples maintained in culture on flow-through diffusion cells for at least 24 h was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and by histological observations. Transepidermal water loss (TEWL) measurements and kinetic analysis of the permeation of both tritiated water and 14C caffeine through the skin were performed after full-spectrum solar exposure involving the use of a xenon arc solar simulator. After a UV exposure of less than 420 mJ/cm2, skin integrity and permeation of both water and caffeine did not change significantly.

Comparison of DNA damage photoinduced by ketoprofen, fenofibric acid and benzophenone via electron and energy transfer.

Ketoprofen (KP) and fenofibrate, respectively, anti-inflammatory and hypolipidemiant agents, promote anormal photosensitivity in patients and may induce photoallergic cross-reactions correlated to their benzophenone-like structure. Here, their ability to photosensitize the degradation of biological targets was particularly investigated in DNA. The photosensitization of DNA damage by KP and fenofibric acid (FB), the main metabolite of fenofibrate, and their parent compound, benzophenone (BZ), was examined on a 32P-end-labeled synthetic oligonucleotide in phosphate-buffered solution using gel sequencing experiments.

Mechanism of DNA damage photosensitized by trisbipyrazyl ruthenium complex. Unusual role of Cu/Zn superoxide dismutase.

Trisbipyrazyl ruthenium(II) (Ru[bpz]3(2+)) was examined as DNA photosensitizer. Damage resulting from the photolysis of synthetic oligonucleotides has been monitored by polyacrylamide gel electrophoresis. Photoadduct formation is found on both single- and double-stranded oligonucleotides.

Pyropheophorbide-a methyl ester-mediated photosensitization activates transcription factor NF-kappaB through the interleukin-1 receptor-dependent signaling pathway.

Pyropheophorbide-a methyl ester (PPME) is a second generation of photosensitizers used in photodynamic therapy. We demonstrated that PPME photosensitization activated NF-kappaB transcription factor in colon cancer cells. Unexpectedly, this activation occurred in two separate waves, i.

Comparison of the DNA damage photoinduced by fenofibrate and ketoprofen, two phototoxic drugs of parent structure.

Fenofibrate and ketoprofen (KP) are two drugs of similar structure derived from that of benzophenone. Both are photoallergic and promote cross reactions in patients. However, the cutaneous photosensitizing properties of KP also include phototoxic effects and are more frequently mentioned.

Nonsteroidal antiinflammatory drug-photosensitized formation of pyrimidine dimer in DNA.

Phototoxic nonsteroidal antiinflammatory drugs (NSAIDs) may induce DNA damage in vitro upon irradiation. In this study, we investigated the ability of ketoprofen (KP), tiaprofenic acid (Tia), naproxen (NP) and indomethacin (IND) to photosensitize the formation of pyrimidine dimers and single strand breaks. Both kinds of damage were sought by analyzing DNA-drug mixtures irradiated at 313 nm by agarose gel electrophoresis.

Comparative study of Ru(bpz)3(2+) Ru(bipy)3(2+) and Ru(bpz)2Cl2 as photosensitizers of DNA cleavage and adduct formation.

The efficiency of ruthenium complexes for photosensitizing DNA damage depends on the oxidizing character of their ligands. Here we report on the difference in behavior of tris(2.2'-bipyrazyl)ruthenium(II) (Ru[bpz]3(2+)), tris(2,2'-bipyridyl)ruthenium(II) (Ru[bipy]3(2+)) and cis-dichlorobis (2,2'-bipyrazyl)ruthenium(II) (Ru[bpz]2Cl2).

Tuning the mechanism of DNA cleavage photosensitized by ruthenium dipyridophenazine complexes by varying the structure of the two non intercalating ligands.

The influence of the nature of ligands on the efficiency of ruthenium complexes for photosensitizing DNA cleavage was investigated. Ru(bipy)2dppz2+ and Ru(bpz)2dppz2+ were selected as DNA breakers on the basis of their high affinity for DNA due to the presence of a dppz ligand which can partially intercalate in the major groove of DNA. Their photosensitizing properties were compared to those of Ru(bipy)3(2+), a complex which binds to DNA with a far lower constant.

Interest of photochemical methods for induction of lipid peroxidation.

Lipid peroxidation, which plays a part in a wide variety of biological processes, is an integral process in the oxidation of unsaturated fatty acids via a radical chain reaction. Among the various species which may induce this reaction in vivo, reactive forms of oxygen such as peroxide anion, the hydroxyl radical and singlet oxygen are of cardinal importance. These species may be generated enzymatically, chemically or by various radiochemical and photochemical reactions.

DNA cleavage photoinduced by new water-soluble zinc porphyrins linked to 9-methoxyellipticine.

Two hybrid molecules based on a water-soluble zinc porphyrin covalently linked to 9-methoxyellipticine, 1 and 2, were studied as photoactivable DNA cleavers. The behaviour and efficiency of these photosensitizers were compared with the constitutive units of the hybrid molecules: meso-tetrakis(4-N-methylpyridiniumyl)porphyrinato-zinc(II) tetraacetate (ZnTMPyP, 3) and 9-methoxy-N2methylellipticinium acetate (9-OMe-NME, 4). On irradiation at 436 nm, the efficiency of these hybrids is similar to that of ZnTMPyP and 50-fold greater than that of haematoporphyrin derivative (HPD).

Interactions of amiodarone with model membranes and amiodarone-photoinduced peroxidation of lipids.

The potent antiarrhythmic drug, amiodarone (AMIO) exhibits phototoxicity, which is thought to be related to its interaction with biological membranes. We report here a spectroscopic study of the interactions of this drug with phosphatidylglycerol (PG) and phosphatidylcholine (PC) liposomes used as membrane model systems. A linear increase in absorbance at 300 nm was observed with increasing addition of AMIO to dimyristoyl-DL-PC (DMPC) liposomes over all the drugs-lipid molar ratio (Ri)s tested.

Wavelength dependence of photoinduced peroxidation and cytotoxicity of human low density lipoproteins.

The relative abilities of UV-A, B and C radiations to initiate lipid peroxidation and apolipoprotein (apo) B modification of human purified low density lipoproteins have been compared. Ultraviolet-B and C (at 310 and 254 nm, respectively) exhibited similar efficacy as shown by the increase in lipid peroxidation markers (conjugated dienes, thiobarbituric acid reactive substances and fluorescent lipid soluble products) and in oxysterols, as well as by the decrease of the contents of natural antioxidants (tocopherols and carotenes) and in polyunsaturated fatty acids. In contrast, UV-A (at 360 nm) was found poorly effective and only at very high radiation intensities.

Mechanism of DNA cleavage mediated by photoexcited non-steroidal antiinflammatory drugs.

DNA damage photoinduced by four nonsteroidal antiinflammatory drugs (NSAID) have been investigated by neutral agarose gel electrophoresis. Upon irradiation at 300 nm, in phosphate buffered solution, benoxaprofen, naproxen, ketoprofen, tiaprofenic acid photosensitized the formation of single-strand breaks (SSB) in double stranded supercoiled phi X174 DNA. The efficiency of the cleavage is higher in argon saturated solutions than in aerated solutions and it is not correlated with the quantum yield of photodegradation of the drugs.

DNA strand breaks photosensitized by benoxaprofen and other non steroidal antiinflammatory agents.

Benoxaprofen, a non steroidal antiinflammatory drug is known to be highly phototoxic. Upon irradiation at 300 nm, benoxaprofen is shown to enhance the cleavage of phi X 174 DNA in buffered aqueous solution (pH 7.4).