摘要:

Abstract—Zn(II)phthalocyanine (ZnPc) generates O2(1Δg) with a quantum yield ofca.0.4 upon photocxcitation at 354 or 600 nm in ethanolic solution as determined by time‐resolved phosphorescence studies at 1270 nm and photooxidation experiments using 1,3‐diphenylisobenzofuran (DPBF) as substrate. The quantum yield of photooxidation slightly increases upon incorporation of ZnPc into unilamellar liposomes of dipalmitoylphosphatidylcholine. Under our irradiation conditions (600 nm, 18°C, and short light exposure times), DPBF(5–50μM)undergoes photooxidation by a pure Type II mechanism; the rate constant for the O2(1Δg) + DPBF reaction is (1.1 ±0.1) x 109M‐1s_1in ethanol solution and determined to be about two orders of magnitude smaller when both ZnPc and DPBF are embedded

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02778.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—Fluorescence lifetimes of 3‐methyllumichrome dual fluorescence at 440 nm (alloxazinic) and 520 nm (isoalloxazinic) and of 1,3‐dimethyllumichrome, which is unable to phototautomerize, at the same wavelengths have been measured in methanol‐acetic acid mixtures. The fluorescence decays of both lumichromes studied are exponential and the phototautomeric fluorescence of 3‐methyllumichrome is created within approximately 50 ps. From the initial values of about 0.9 ns (alloxazinic) and 6.4 ns (isoalloxazinic) in 5% acetic acid the lifetimes shorten considerably with increasing acid concentration reaching 0.2 ns for 1,3‐dimethyllumichrome and 80 ps for the alloxazinic and 2.4 ns for the isoalloxazinic form of 3‐methyllumichrome in pure acid. Static and dynamic fluorescence quenching constants were estimated. The differences in the quenching rate and equilibrium constants of both lumichromes are interpreted in terms of different equilibria of hydrogen bond formation in ground and excited state as influenced by steric effects of the methyl substituent at the N‐l position in 1,3‐dimethyl. The hydrogen bonding atN–10 of 3‐methyllumichrome with acetic acid is a prerequisite for additional hydrogen bonding at N‐l enabling excite

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02779.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—The quenching of the fluorescence emitted by hematoporphyrin incorporated into unilamellar liposomes of dipalmitoyl‐phosphatidylcholine and dimyristoyl‐phosphatidylcholine, was studied by using methylviologen, 9,10‐anthraquinone‐2,6‐disulfonate and 9,10‐anthraquinone‐2‐sulfonate as quenchers, in order to assess how the distribution of the porphyrin and the interaction mode of the various quenchers with the porphyrin is affected by the physico‐chemical properties of the vesicles.The results obtained indicate that, below the critical temperature for the phase transition of the lipids, hematoporphyrin is preferentially distributed in the outer lipid monolayer of liposomes of dipalmitoyl‐phosphatidylcholine while most hematoporphyrin molecules are located in the inner monolayer in liposomes of dimyristoyl‐phosphatidylcholine. This distribution is only slightly changed when the external mean radius of liposomes increases from 26 to 50 nm.The rise of temperature above the critical value for the liquid‐gel phase transition causes a shift of the hematoporphyrin molecules toward the inner phospholipid monolayer. This shift is more pronounced in liposomes of dimyristoyl‐phosphatidylcholine.Studies on model systems, i.e. neutral and ionic micelles, indicate that methylviologen and anthra‐quinone‐type quenchers drastically differ in their interaction mechanism with hematoporphyrin. In particular, methylviologen is the only quencher which can discriminate different hematoporphyrin populations in liposomes of dimyristoyl‐phosphatidylcholine and dipalmitoyl‐phosphatidylcholine in both the liquid and gel phase. Anthraquinone‐type quenchers interact with both hematoporphyrin populations when the lipids are in the gel phase. When the lipids are in a fluid state, the quenching occurs only on the external hematoporphyrin population in liposomes of dipalmitoyl‐phosphatidylcho‐line while in liposomes of dimyristoyl‐phosphatidylcholine no discrimination is observed. The influence of the liposomal structure at different temperatures and of the le

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02780.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—The 1,4‐diamino‐substituted anthraquinones mitoxantrone and ametantrone do not photosensitize DNA damage following illumination with visible light. In contrast, both the 1,5‐ and 1,8‐bis[[(diethylamino)ethyl]amino]anthraquinones, AMI and AM2 respectively, sensitized DNA single‐strand break formation in closed‐circular plasmid DNA upon exposure to visible light. The presence of an electron donor such as NADH is required in the case of AMI, and enhances the effect with AM2. At increasing DNA base pair to drug ratios the rate of oxygen consumption decreased rapidly suggesting that the drug photosensitizing properties are lost upon binding or intercalation into DNA. A direct correlation between oxygen consumption, NADH oxidation and extent of DNA damage was established at different DNA base pair t

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02781.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—Single‐strand break formation and biological deactivation of plasmid pBR322 DNA in the presence of tris(2,2′‐bipyridyl)‐ruthenium(II), Ru(bpy)2/3;+, and K2S2O8, upon irradiation with visible light(400–500 nm), were studied in aqueous solution at room temperature. Conditions of complete binding of Ru(bpy)2/3;+to the strand were employed. The damage is initiated mainly by the SO2/3;; radical anion. Under anoxic conditions at a ratio of nucleotide to sensitizer concentrations (N/S) of 18 and S2O2/8‐concentrations of 0.5mMthe quantum yield of single‐strand break (ssb) formation is φssb= 8.4 times 10‐3while that of biological deactivation (bd) is Øbd= 7.6 times 10‐3(φssb= 5.2 times 10‐36.4 times 10‐3, 6.0 times 10‐3and φbd= 4.2 times 10‐3, 5.2 times 10‐3, 4.8 times 10‐3at N/S=3, 6, and 9, respectively). The quantum yields are approximately 2.5 times smaller in air‐saturated solutions. At N/S = 18 about 33 SO4‐radical anions are required per one lethal event. φbdincreases linearly with the S2Oφ‐concentration (up to 0.5mM).The damage to DNA is drastically reduced on addition of mono‐ or divalent salts (e.g. NaC104, MgCl2). These additives cause the release of Ru(bpy)2+from the strand. The observed damage to DNA is thus the result of a site specific reaction. When the phenanthroline analogue, Ru(phen)φ+, is used as

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02782.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—DNA purine modifications by ultraviolet irradiation have not been as extensively studied as those of pyrimidines. However, a number of such reactions have been identified. These include photochemical addition of amino acids, photoalkylation by alcohols, amines and other compounds, photochemical activation of procarcinogens to mutagenic electrophiles, and formation of covalent linkages between DNA purines and adjacent bases. The recent characterization of two adenine‐adenine di‐adducts and the finding of endonucleases from two sources that incise ultraviolet‐irradiated DNA at purine photoproducts indicate the possible biological importance of these m

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02783.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—The relative biological importance of(5–5,6–6) cyclobutane and(6–4) pyrimidine‐pyrimidone dimers in mammalian cells has been determined in a xeroderma pigmentosum (XP) revertant that repairs only the(6–4) photoproduct. Surprisingly, the majority of biological effects of UV light, including cell killing, sister chromatid exchange, mutagenesis, and inhibition and recovery of DNA and RNA synthesis, appear to be due to the(6–4) photoproduct and not to the cyclobutane dimer. Although the XP revertant repairs its own genomic DNA, it fails to repair damage in shuttle vectors, including the pZ189 mutational and chloramphenicol acetyl transferase transcriptional assay systems. The revertant is therefore a cell line for which shuttle vectors are inappropriate as models for genomic DNA repair, and may highlight a general weakness of shuttle vectors for the study of infrequen

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02784.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—The significance of the pyrimidine(6‐4)pyrimidone photoproduct in mammalian cell killing is considered. Photochemical data indicate that the(6–4) photoproduct is induced at a substantial frequency compared to the cyclobutane dimer and that the action spectra for the induction of both lesions are equivalent. The repair of(6–4) photoproducts in various normal and UV‐hypcrsensitive mammalian cell lines, including several recently derived somatic cell hybrids and transformants, is presented. The sensitivity of these cells to ultraviolet irradiation correlates better with the capacity to repair(6–4) photoproducts than cyclobutane dimers. These data are used to support that idea that the(6–4) photoproduct is one of the major cytotoxic lesions induced in DNA by ultr

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02785.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—The relevance of photoproducts produced by 254 nm irradiation to human skin cancer is first critically evaluated. Experiments identifying the mutagenic photoproducts at 254 nm are then described. Mutations are primarily due to the(6–4) photoproduct and the cyclobutane pyrimidine dimer, both inE. coliand in human cells. The(6–4) photoproduct may be more important inE. coliand the cyclobutane dimer more important in mammalian cells. In human cells, mutations occur at the C of a TC, CT, or CC cyclobutane dimer, but not at TT cyclobutane dimers, and also appear to occur, less frequently, at the C of TC and CC(6–4) photoproducts. The local structure of DNA is more important in determining the frequency of mutation at a site than is the photoproduct frequency at that site. The effect of DNA structure appears to be due to site‐specific

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02786.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

Abstract—Ultraviolet light causes a type of damage to the DNA of human cells that results in a DNA strand break upon subsequent irradiation with wavelengths around 300 nm. This DNA damage disappears from normal human fibroblasts within 5 h, but not from pyrimidine dimer excision repair deficient xeroderma pigmentosum group A cells or from excision proficient xeroderma pigmentosum variant cells. The apparent lack of repair of the ultraviolet light DNA damage described here may contribute to the cancer prone nature of xeroderma pigmentosum variant individuals. These experiments show that the same amount of damage was produced at 0°C and 37°C indicating a photodynamic effect and not an enzymatic reaction. The disappearance of the photosensitive lesions from the DNA is probably enzymatic since none of the damage was removed at 0°C. Both the formation of the lesion and its photolysis by near ultraviolet light were wavelength dependent. An action spectrum for the formation of photosensitive lesions was similar to that for the formation of pyrimidine dimers and(6–4) photoproducts and included wavelengths found in sunlight. The DNA containing the lesions was sensitive to wavelengths from 304 to 340 nm with a maximum at 313 to 317 nm. This wavelength dependence of photolysis is similar to the absorption and photolysis spectra of the pyrimidine(6–4) phot

ISSN:0031-8655    

DOI:10.1111/j.1751-1097.1988.tb02787.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY