Disease relevance of Dermatitis, Phototoxic

• These in vivo results extend our previous in vitro observation of photoactivation of complement in sera from patients with erythropoietic protoporphyria and porphyria cutanea tarda, and suggest that the complement system may participate in the pathogenesis of cutaneous phototoxicity in these patients [1].
• These results indicate that superoxide, hydrogen peroxide, and the hydroxyl radical are generated by illuminated tetracyclines and are molecular agents of tetracycline phototoxicity in E. coli B [2].
• The Artemia salina method proved to be rapid, simple and inexpensive, and is therefore ideal in the initial biological screening of large numbers of samples for simultaneous detection of both toxicity and phototoxicity [3].
• Ketoprofen (3-benzoyl-alpha-methylbenzeneacetic acid, KP) is a widely used nonsteroidal anti-inflammatory drug (NSAID) that causes both phototoxicity and photoallergy [4].
• The blistering, which resembles that occurring in nalidixic acid phototoxicity and in porphyria cutanea tarda, is considered phototoxic in nature [5].

High impact information on Dermatitis, Phototoxic

• Role of complement and polymorphonuclear cells in demethylchlortetracycline-induced phototoxicity in guinea pigs. Inhibition by decomplementation in vivo [6].
• In the series demeclocycline, tetracycline, and minocycline, the efficiency of singlet oxygen generation is found to parallel the clinical observation of relative frequency of phototoxicity of these antibiotics, suggesting singlet oxygen generation as the origin of their phototoxicity [7].
• Phototoxicity of the tetracyclines: photosensitized emission of singlet delta dioxygen [7].
• Phototoxicity, as measured by a clonogenic assay and by uptake of ethidium bromide, was dependent on the doses of both mAb-chlorin and 630- to 670-nm light, was enhanced by 2H2O, and was observed only in target populations that bound the mAb [8].
• These observations suggest that sustained ERK1/2 activation protects cells from Photofrin-mediated phototoxicity and that the duration of ERK1/2 activation is regulated by MKP-1 [9].

Chemical compound and disease context of Dermatitis, Phototoxic

• The implications of our results in connection with the relevance of oxygen-dependent photoreactions of chlorpromazine to its phototoxicity, and the possible appearance of hepatic alterations in patients treated with the drug after exposure to the sunlight, are discussed [10].
• Due to problems of prolonged skin phototoxicity with hematoporphyrin derivative, new photosensitizers and methods of localization are being sought [11].
• The phototoxicity in vitro of rhodamine 123 and tetrabromo rhodamine 123 (TBR) was compared, in order to assess their photochemotherapeutic potential [12].
• Irradiation of MGH-U1 cells in the presence of the glutathione depleter buthionine sulfoximine also increased the phototoxicity, demonstrating a role for intracellular glutathione and possibly free radical intermediates [11].
• This result shows that diaziquone can catalyze phototoxicity; the action spectrum of the drug may limit clinical applications of this phenomenon [13].

Biological context of Dermatitis, Phototoxic

• Of the three drugs, fluphenazine exhibited the highest phototoxicity and 100% cell death was achieved with a light dose of 5 J/cm2 [14].
• Methylene blue phototoxicity may be related to the high prenatal dose of the dye relative to patient's small size and young gestational age [15].
• Irradiation of L1210 cells in the presence of N-hydroxypyridine-2(1H)-thione, a nonspecific, photochemical source of hydroxyl radical, was also found to trigger phototoxicity and lipid peroxidation [16].
• Quantitative structure-activity relationship analysis of thiophene phototoxicity suggested that the rate of singlet oxygen production is the primary determinant of antiviral and cytotoxic activities [17].
• After 2 h incubation of RIF-1 cells with the phototoxicity LD50 concentration, methylene blue and all analogues were observed to be localized in the lysosomes by fluorescence microscopy [18].

Anatomical context of Dermatitis, Phototoxic

• The phototoxicity mechanism of a kryptocyanine dye, N,N'-bis(2-ethyl-1,3-dioxolane)kryptocyanine (EDKC+), has been studied in RBC membranes and isolated mitochondria [19].
• Adaptive antioxidant response protects dermal fibroblasts from UVA-induced phototoxicity [20].
• Inhibition of myeloperoxidase activity with 4-aminobenzoic acid hydrazide (4-ABAH) had minimal influence on the phototoxicity of VP in HL-60 cells in the absence of ascorbate [21].
• In vivo mediator release and degranulation of mast cells in hematoporphyrin derivative-induced phototoxicity in mice [22].
• Photosensitizer entrapped in PCLs showed enhanced phototoxicity for a human vascular endothelial cell line, ECV304, in comparison with that for nonmodified control liposome [23].

Gene context of Dermatitis, Phototoxic

• Glutathione peroxidase activities were elevated following irradiation but returned to control levels within 0.5 h for both doses, implicating hydroperoxide formation as an early event in hypericin phototoxicity [24].
• The green tea constituent (-)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant and has shown remarkable preventive effects against photocarcinogenesis and phototoxicity in mouse models [25].
• Preparation, phototoxicity and biodistribution studies of anti-carcinoembryonic antigen monoclonal antibody-phthalocyanine conjugates [26].
• Phototoxicity was essentially identical in hisC3076, hisD3052 and hisG46 strains; uvrB- excision-repair-deficient bacteria were considerably more susceptible to lethal effects than wild-type parental strains, while the presence of pKM101 had no apparent effect on survival [27].
• STUDY DESIGN/MATERIALS AND METHODS: CPAE, PTK2, and rat neonatal myocardial cells treated with ALA were examined for localization using fluorescence microscopy and for subcellular phototoxicity using 630 nm laser microbeam irradiation of specific subcellular regions [28].

Analytical, diagnostic and therapeutic context of Dermatitis, Phototoxic

• This study describes an adaptation of this strategy for the delivery of chloroaluminum phthalocyanine tetrasulfonate ([AlPcS(4)](4-)), a water-soluble sensitizer used in photodynamic therapy, in a binary targeting scheme designed to enhance both its tumor selectivity and phototoxicity [29].
• Cell cultures in the investigation of thiazide phototoxicity [30].
• The cytotoxicity (in the dark), phototoxicity (red light) and subcellular localization (using confocal laser scanning microscopy) were determined for 15 porphyrins (1-15) in C6 glioma cells [31].
• The observed phototoxicity makes curcumin a potential photosensitizing drug which might find application in the phototherapy of, for example, psoriasis, cancer, and bacterial and viral diseases [32].
• ESR studies of a series of phthalocyanines. Mechanism of phototoxicity. Comparative quantitation of O2-. using ESR spin-trapping and cytochrome c reduction techniques [33].

References