三嗪类化合物的合成及其产酸性能研究

合成了一系列的三嗪类光生酸剂1a—1e,确定了它们的结构,并对1e在乙腈溶剂中365和405nm光下的曝光分解产酸性能进行了初步的定量研究.结果表明,在测定浓度范围内分解量子产率和产酸量子产率基本上都不随浓度的变化而变化,在405nm光下比在365nm光下有更高的分解和产酸量子效率.有关这类化合物的光生酸性能与曝光波长的关系正在进一步研究中.     

新型锍鎓盐类光生酸剂的合成及产酸性能研究

成功合成了两种新型锍鎓盐类光生酸剂,其结构经¹1HNMR和MS分析确认,并对其基本物性及在405、365nm光下乙腈溶液中的分解及产酸性能进行了研究,通过计算得出了分解及产酸量子产率.结果表明,两种化合物有较高的热分解温度和在常用有机溶剂中有较好的溶解性;在405nm光源下,4-(9′-苯基蒽基)苯基三氟甲磺酸锍鎓盐(PAGS1)和4-(4′-N,N-二乙基-1′-苯乙烯基)苯基三氟甲磺酸锍鎓盐(PAGS2)的分解量子产率分别为10%和15%,产酸量子产率为8.1%和13%;但在365nm光源下,分解及产酸量子产率均很低,说明两种光生酸剂对于405nm波长的光较敏感,适宜作为405nm光源下的光生酸剂.     

水溶性二苯酮类光敏剂中的羟基对光谱和光聚合的影响

有许多公司和研究所在从事光聚合的研究.本文报导两种不同分子结构的水溶性光敏剂的紫外光谱、磷光光谱和在不同溶剂中的量子产率,比较它们在水溶性预聚体中的光聚合效应. 两种水溶性光敏剂为:     

4-n-壬基酚的激光闪光光解和紫外光降解

采用266nm激光闪光光解瞬态吸收光谱和254nm紫外光降解,研究了乙腈及乙腈-水混合溶液中4-n-壬基酚（4-n-NP）的各种光解行为,考察了不同物理化学体系对4-n-NP光解行为的影响规律.实验发现,在266nm激光闪光光解下,4-n-NP既发生光电离又发生光激发,获得了4-n-NP光电离生成的阳离子自由基,以及光激发生成的激发三重态的瞬态特征吸收谱.由S2O82-光分解产生的SO4·-可快速氧化4-n-NP,测得反应速率常数为2.85×109M-1s-1,判定4-n-NP阳离子自由基在pH高于2.2条件下会转变成脱质子中性自由基.研究发现,使用254nm紫外光直接降解4-n-NP比较困难,UV结合添加H2O2可提高其降解效率,UV结合添加K2S2O8可极大提高4-n-NP降解效率,3.5min的光照即可使1×10-4M的4-n-NP完全降解.本文就4-n-NP在各种条件下的光解机理进行了探讨,为此类具有生物激素效应的非离子表面活性剂光降解奠定了基础.     

酸敏变色记录显示片再生方法的研究

我们进行了酸敏变色记录显示片(简称酸敏片)重复使用的试验,并对其实用性在实验中给予证实。实验结果表明:酸敏片经曝光后,由于释放 HCI 酸源使酸性指示剂变色形成图像,通过还原酸性指示剂,使曝     

X射线光电子能谱法研究UV_(254nm)光催化、O_3强化UV_(254nm)光催化和真空紫外光催化降解甲醛中Pt-TiO_2薄膜的表面性质(英文)

以Pt-TiO2为光催化剂,研究了气相甲醛分别在35 h连续UV254 nm光催化、O3强化UV254 nm(O3+UV254 nm)光催化和真空紫外(UV254+185 nm)光催化中的降解效率,考察了副产物O3的去除率,采用X射线光电子能谱(XPS)法分析Pt-TiO2在不同光催化前后Pt的电子态和累积有机产物,研究纳米Pt对甲醛降解和O3去除的强化机理.连续光催化降解实验表明,以纳米Pt改性TiO2可以同时增强甲醛和O3的去除率,特别是O3的去除率可提高3.1–3.4倍.对催化剂C 1s和O 1s峰分别经分峰拟合处理后,发现Pt-TiO2上累积的含羰基和羟基的有机物含量按以下顺序减少:UV254 nm光催化O3强化UV254 nm光催化真空紫外光催化,而在连续35 h光催化降解过程中,催化剂的失活现象却按相反的方向变得越来越不明显.负载的金属Pt在O3+UV254 nm和UV254+185nm光催化过程中被氧化成PtOads和Pt4+物种,而在UV254 nm光催化过程中金属Pt未被氧化,所以推测是气相中的O3和羟基自由基参与金属Pt的氧化过程.Pt-TiO2表面高价态的Pt氧化物种可作为光生电子捕获中心,强化光生载流子的分离过程,增强Pt-TiO2的光催化活性.Pt氧化物种可作为O3分解的活化中心,使Pt-TiO2对O3的分解效率远高于纯TiO2.以XPS对比研究在三种不同光催化环境中Pt-TiO2表面性质,可以解释在UV254+185 nm光催化过程中纳米Pt对甲醛和O3同时去除的强化机理,并说明了催化剂不失活的内在原因.     

一种高感度深紫外正性化学增幅型抗蚀剂的制备

聚对羟基苯乙烯和环己基乙烯基醚反应得到缩醛保护的聚合物.该聚合物易溶于常见的有机溶剂,具有较好的热稳定性,在248 nm处透明性良好.该聚合物可与聚对羟基苯乙烯-甲基丙烯酸金刚烷基酯及二砜光产酸剂等组成一种三组分正性化学增幅型深紫外光致抗蚀剂,初步研究了该抗蚀剂的感光成像性能.采用KrF激光（248 nm）曝光,在较低的后烘温度下,显影得到分辨率为180 nm的线条图形.显影后的留膜率在99%以上.在光致抗蚀剂体系中引入对羟基苯乙烯-金刚烷基甲基丙烯酸酯共聚物,可提高光刻胶材料的玻璃化转变温度,有利于其实际应用.     

铝片表面阳极氧化铝膜的光催化作用

采用阳极电化学氧化在铝片表面制备出表面含有氧化铝膜的铝片(AAO/Al), 分别用FTIR-ATR技术和密闭间歇式反应装置考察了该样片对油酸和乙烯的光解作用, 结合UV-DRS和FTIR表征结果对薄膜在油酸和乙烯光解中的作用进行了探讨. 结果表明：AAO/Al能够吸收小于265 nm的紫外光, 而无AAO膜的铝片对波长大于220 nm的紫外光没有任何吸收；254 nm紫外光照射下AAO/Al对油酸和乙烯的光解具有明显的促进作用, 光照3 h油酸的分解率达到70%, 乙烯也有9%的分解, 但相同条件下在无AAO膜的铝片上, 油酸的光解率仅为30%, 乙烯几乎不分解；然而, 在365 nm紫外光照射下, AAO/Al同纯铝片一样对两反应物的光解都没有任何促进作用. 分析认为, AAO膜能吸收254 nm的紫外光和对有机物分解具有光催化作用的可能原因是在AAO膜结构中存在过量的Al原子和氧空位.     

一种新型深紫外正型光致抗蚀剂材料的研究

通过松香酸和丙烯酸的Diels-Alder反应得到了一种二酸——丙烯海松酸.丙烯海松酸有大的脂环结构和良好的成膜性,在固体膜层中,它可以和二乙烯基醚,如1,3-二乙烯氧基乙氧基苯,在加热条件下(80℃以上)发生反应,产物在稀碱水中难溶.这样形成的产物在光产酸剂产生的强酸催化下,在温度高于100℃时,可以迅速分解,从而变成稀碱水易溶.因此,用此二酸、二乙烯基醚和产酸剂可组成一种正型的光致抗蚀剂,当用254 nm的低压汞灯曝光时,其感度在30 mJ/cm²以下.     

磺酸肟酯类光产酸剂的制备及性能研究

本文合成了4种磺酸肟酯类非离子型光产酸剂,用核磁氢谱确认了产物结构,并测试了其热稳定性、紫外吸收特性及产酸效率.结果表明,合成的4种磺酸肟酯类光产酸剂在350-450 nm和深紫外区(DUV,248 nm)都有很好的吸收,在420 nm波段曝光下,(5-对三氟甲基苯磺酸酯亚胺-5H-噻吩-2-亚胺)-苯乙腈(P-2)产酸率最高,可达0.96;(5-对甲基苯磺酸酯亚胺-5H-噻吩-2-亚胺)-苯乙腈(P-1)在365 nm和420 nm两个波段下,均有较高的产酸率.利用实时红外(RT-IR)研究了相同浓度下4种光产酸剂对乙烯基醚化合物引发的光聚合动力学,同时研究了光产酸剂浓度对光聚合反应的影响,发现产酸剂浓度为2%时,光照30 s乙烯基醚化合物的双键转化率(DC%)即能达到80%.     

The impact of ultraviolet light on bacterial adhesion to glass and metal oxide-coated surface

Biofouling of glass and quartz surfaces can be reduced when the surface is coated with photocatalytically active metal oxides, such as TiO2 (anatase form) or SnO2. We measured the attachment of eight strains of bacteria to these two metal oxides (TiO2 and SnO2), and to an uncoated glass (control; designated Si-m) before and after exposure to UV light at wavelengths of 254 nm (UVC) or 340 nm UV (UVA). TiO2-coated surfaces were photocatalytically active at both 254 and 340 nm as evidenced by a decrease in the water contact angle of the surface from 59 degrees +/-2 to <5 degrees. The water contact angle of the SnO2 surface was reduced only at 254 nm, while contact angle of the Si-m glass surface was not altered by light of either wavelength. Bacterial adhesion decreased by 10-50% to photocatalyzed glass surfaces. In all cases, bacteria exposed to the UV light were completely killed due to a combination of exposure to UV light and the photocatalytic activity of the glass surfaces. These results show that UV light irradiation of TiO2-coated surfaces can be an effective method of reducing bacterial adhesion.     

Analysis of a photosensitive lesion induced by sunlamp UV greater than 315 nm exposure of 254-nm-irradiated human cells

Normal human skin fibroblasts were exposed to 0-10 J m-2 of 254 nm UV, incubated 0-16 h and then treated with 0-150 kJ m-2 of sunlamp UV greater than 315 nm. For each treatment, the cells were subjected to alkaline elution in order to measure the yield of single strand breaks (ssb) produced. It was found that treatment of 254-nm-irradiated cells with sunlamp UV greater than 315 nm resulted in the production of a higher level of ssb than that produced by separate exposures. Hence, lesions are produced by the 254 nm irradiation that are photolyzed through exposure to sunlamp UV greater than 315 nm. Approximately 50% of these lesions are removed following a 2-4 h incubation of the 254-nm-irradiated cells and nearly complete removal is achieved by 16 h. In addition, the profiles for elutions performed at pH 12.8 with cells exposed to the combined treatment were indicative of the presence of alkali labile sites. The repair kinetics of this lesion and alkaline lability of the photolysis product suggest that this photosensitive lesion may represent pyrimidine(6-4)pyrimidone photoproducts. Hence, this approach may represent a relatively simple and sensitive assay for the measurement of this DNA damage.     

Effect of UV irradiation at defined wavelengths on the tertiary structure of double-stranded covalently closed circular DNA

Double-stranded, covalently closed, supercoiled circular DNA from phage fd (replicative form) was irradiated with increasing doses of UV light at 254 nm, 290 nm, 313 nm and 365 nm, and subjected to electrophoresis on agarose slab gels. Increasing the doses of UV light at 254 and 290 nm promotes a smooth reduction in the electrophoretic mobility of the sample, as would be expected if the major effect of light at these two wavelengths were to induce the formation of photoproducts leading to the unwinding of the double strand. At high doses, UV light at 290 nm introduces single-strand breaks (1.2 kJ m-2 per nick per million phosphodiester bonds). UV light at 313 nm promotes an abrupt change in the electrophoretic mobility, as would be expected if the effect of this wavelength were to induce single-strand breaks, leading to the transformation of the supercoiled molecules in their relaxed form (23 kJ m-2 in order to introduce one nick per million phosphodiester bonds). UV light at 365 nm also promotes single-strand breaks in DNA (140 kJ m-2 per nick per million phosphodiester bonds).     

THE UV ACTION SPECTRA FOR THE CLONE-FORMING ABILITY OF CULTURED HUMAN MELANOCYTES AND KERATINOCYTES

Abstract Melanocytes (skin type 2) and keratinocytes were irradiated with UV light of 254, 297, 302, 312 and 365 nm and the survival was measured. Clone-forming ability was chosen as the parameter for cell survival. Melanocytes were found to be less sensitive to UV light than keratinocytes (a difference of a factor 1.22-1.92 for the UV-C and UV-R wavelengths (254, 297, 301 and 312 nm) and a factor 6.71 for the UV-A wavelength (365 nm). Because melanin does not appear to protect against the induction of pyrimidine dimers the difference between melanocytes and keratinocytes in the UV-C and UV-B region could not be explained by the presence of melanin in the melanocytes. The relatively small difference can be explained by the longer cell cycle of melanocytes, which provides more time for the melanocytes to repair UV damage. In the UV-A region the difference between melanocytes and keratinocytes was much larger, suggesting that besides the longer cell cycle some additional factors must be involved in protection against UV-A light.     

SENSITIVITIES TO MONOCHROMATIC 254-nm AND 365-nm RADIATION OF CLOSELY RELATED STRAINS OF Saccharomyces cerevisiae WITH DIFFERING REPAIR CAPABILITIES

Abstract— Sensitivity to monochromatic 254- and 365-nm radiation was compared in closely related yeast strains with defects in one or more of the excision-repair ( rad1 ), error-prone repair ( rad18 ), or recombinational-repair ( rad51 ) pathways. At 254 nm, mutants defective in a single repair pathway exhibited slight to moderate UV sensitivity; those defective in two separate pathways were somewhat more UV sensitive, while triple mutants defective in all three pathways exhibited extreme UV sensitivity with a lethal event corresponding to 0.05 J m⁻². Repair defects also rendered mutants sensitive to 365-nm radiation; strains with single defects exhibited slight sensitivity, mutants with two defective pathways were more sensitive, and triple mutants exhibited maximal sensitivity with a lethal event corresponding to 2.4 times 10⁴ J m⁻². In the triple mutant ( rad1, rad18, rad51 ) at both 254 and 365 nm, the dose per lethal event was almost identical with comparable values in a repair-deficient double mutant ( uvrA, recA ) of Escherichia coli. In the E. coli mutant pyrimidine dimers are believed to be the primary cause of lethality at both wavelengths. Evidence for dimer involvement in the yeast mutant was obtained by demonstrating that lethality at both 254 and 365 nm was photoreactivated by light at 405 nm.     

LETHALITY IN REPAIR-PROFICIENT ESCHERICHIA COLI AFTER 365 nm ULTRAVIOLET LIGHT IRRADIATION IS DEPENDENT ON FLUENCE RATE

Abstract Reciprocity (total applied fluence produces the same response, regardless of the fiuence rate) for the lethal effects caused by 365 and 254 nm ultraviolet light (UV) was studied for repair-proficient and -deficient Escherichia coli strains. In the repair-proficient strain, E. coli WP2 uvrA * recA *, reciprocity after 365 nm UV was only observed at fluence rates of about 750 Wm^-2 and above. Below this rate, the cells became increasingly sensitive as the fluence rate was decreased. Similar lack of reciprocity was obtained whether the cells were exposed at 0 or 25°C. The double repair-defective mutant, E. coli WP100 uvrA recA , showed complete reciprocity after 365 nm UV over the same range of fluence rates measured for the repair-proficient strain. For 254 nm UV, complete reciprocity occurred in both strains over a range of fluence rates differing by an order of magnitude.     

Investigating the Red Shift between in vitro and in vivo Urocanic Acid Photoisomerization Action Spectra

Abstract— Trans-urocanic acid (UCA) is found in the upper layer of the skin and UV irradiation induces its photoisomerization to cis -UCA. Cis -UCA mimics some of the immunosuppressive properties of UV exposure. The wavelength dependence for in vitro photoisomerization of trans-UCA (15 μM) over the spectral range 250 nm-340 nm (10 nm intervals) was determined. The action spectrum revealed that maximal cis-UCA production occurred at 280 nm, which is red-shifted by 10-12 nm from its absorption peak at 268 nm and differs markedly from the reported action spectra for cis-UCA production in mouse skin in vivo , which peaks at 300-310 nm. The reasons for the red shift between the in vitro and in vivo action spectra are not clear. There is limited evidence suggesting that the UV absorption maximum of trans- UCA red shifts from 268 nm in vitro to 310 nm on interaction with stratum corneum proteins in vivo. This phenomenon was investigated by applying trans-UCA (2.5 mg/cm²) in an oil emulsion to isolated human stratum corneum. After incubation at 37°C for 1 h, the absorption spectra of stratum corneum with UCA and with oil only were compared using a Xe arc source and a spectrora-diometer. A moderate red shift in trans-UCA absorption from ∼268 nm to 280 nm was observed. In summary, we suggest that the 10-12 nm red shift between the UCA absorption spectrum peak and the action spectrum peak in vitro may be accounted for by the wavelength dependence of quantum yields reported over the 254-313 nm range. The red shift between the in vitro and in vivo photoisomerization action spectra may result from the 10 to 12 nm red shift in the absorption of UCA in association with stratum corneum proteins, combined with increasing quantum yields over the 254-313 nm range.     

Primary photochemical processes of the phototoxic neuroleptic cyamemazine: a study by laser flash photolysis and steady-state irradiation

The photophysical and photochemical properties of the UV-A-absorbing phototoxic drug cyamemazine (CMZ) (2-cyano-10-(3-[dimethylamino]-2-methyl-propyl)-phenothiazine) have been investigated in neutral buffered aqueous solutions. The transient absorbances of the hydrated electrons, of the first excited triplet state (3CMZ*) with a characteristic absorption band peaking at 420 nm and of the radical cation (*CMZ+) (maximum absorbance at 500 nm) have been observed by 355 nm laser flash spectroscopy of deaerated solutions. All these transient species are formed by monophotonic processes and react with oxygen. Bimolecular reaction rate constants of *CMZ+ and 3CMZ* with O2 are 2 x 10(7) M(-1) s(-1) and 4 x 10(9) M(-1) s(-1), respectively. The 3CMZ* reacts only sluggishly (reaction rate constant, 9 x 10(6) M(-1) s(-1)) with tryptophan chosen as a Type-I photodynamic substrate. Steady-state irradiations with 365 nm light demonstrate that CMZ is rapidly photolyzed (quantum yield, 0.04) in O2-saturated solutions leading to oxidation of the sulfur atom and of the side-chain nitrogen of CMZ. This photoproduct (2-cyano-10-(3-[dimethylamino, N-oxide]-2-methyl-propyl)-5-oxide-phenothiazine), is a good Type-I and Type-II photodynamic photosensitizer producing singlet oxygen in high yield (approximately 0.45) and could play a major role in the phototoxicity of CMZ.     

ULTRAVIOLET LIGHT IRRADIATION OF DEFINED-SEQUENCE DNA UNDER CONDITIONS OF CHEMICAL PHOTOSENSITIZATION

Abstract— The formation of cyclobutane pyrimidine dimers and UV light-induced (6-4) products was examined under conditions of triplet state photosensitization. DNA fragments of defined sequence were irradiated with 313 nm light in the presence of either acetone qr silver ion. UV irradiation in the presence of both silver ion and acetone enhanced the formation of TT cyclobutane dimers, yet no (6-4) photoproducts were formed at appreciable levels. When photoproduct formation was also measured in pyrimidine dinucleotides, only cyclobutane dimers were formed when the dinucleotides were exposed to 313 nm light in the presence of photosensitizer. The relative distribution of each type of cyclobutane dimer formed was compared for DNA fragments that were irradiated with 254, 313, or 313 nm UV light in the presence of acetone. The dimer distribution for DNA irradiated with 254 and 313 nm UV light were very similar, whereas the distribution for DNA irradiated with 313 nm light in the presence of acetone favored TT dimers. Alkaline labile lesions at guanine sites were also seen when DNA was irradiated with 313 nm light in the presence of acetone.