THE INACTIVATION OF RIBONUCLEIC ACID FROM TOBACCO MOSAIC VIRUS BY ULTRAVIOLET RADIATION AT DIFFERENT WAVE-LENGTHS

Abstract— Although both thymine and uracil can form similar dimers, exposing RNA of tobacco mosaic virus lo ultraviolet radiation of different wavelengths did not reproduce any of the phenomena that implicate dimerization of thymine residues as a major cause of the inactivation of a bacterial transforming DNA. If uracil residues dimerize at all in the irradiated RNA, such dimerization either does not affect infectivity or is not photoreversible in the same way as dirnerization of thymine residues in DNA. Unlike inactivation of the transforming DNA, inactivation of the virus-RNA seems to be a function of the amount of absorbed radiation energy, irrespective of the wave-length within the range 285 to 230 mμ and irrespective of a change in the wave-length during irradiation.     

INACTIVATION BY ULTRAVIOLET RADIATION AT DIFFERENT WAVELENGTHS OF THE RNA ISOLATED FROM POTATO VIRUS X

Abstract— –The action spectra and quantum yields for photoreactivable, non-photoreactivable and total damage caused by u.v. in the RNA isolated from potato virus X differ from those for similar types of damage in the whole virus. The differences result from the virus protein partly protecting the RNA from damage, and the degree of protection depends on the wavelength of u.v. and on the salt concentration of the irradiated solution. The action spectra for the different types of damage in the RNA all resemble the absorption spectrum of the RNA, but do not exactly parallel it. The photoreactivable sectors of the RNA and of the whole virus are greater at 290 nm than at 230 nm but, whereas that of the virus increases rectilinearly, that of the RNA has a pronounced minimum at about 250 nm. At wavelengths longer than 240 nm, the photoreactivable sector of the virus exceeds that of the RNA, because, at these wavelengths, the virus protein protects the RNA more against non-photoreactivable damage than against photoreactivable damage.     

IN ACTIVATION OF A STRAIN OF TOBACCO NECROSIS VIRUS AND OF THE RNA ISOLATED FROM IT, BY ULTRAVIOLET RADIATION OF DIFFERENT WAVE-LENGTHS

Abstract— A train of tobacco necrosis virus (TNV) and infective nucleic acid isolated from it (TNV-RNA) are equally susceptible to inactivation by U.V. radiation at all wave-lengths tested (230-290 m_μ) and can be photoreactivated to the same extent by exposing inoculated host plants to daylight. The shape of the action spectrum for inactivation by U.V. of TNV and of TNV-RNA follows that of the absorption spectrum of TNV-RNA. Thus, unlike the RNA of tobacco mosaic virus, the RNA of TNV behaves in all these respects in the same way irrespective of whether it is inside or outside the virus particle. To inactivate TNV or TNV-RNA to 50 per cent of their original infectivities, each mg of RNA must absorb about 0.27 joules of radiation energy of any wave-length between 230 and 290 mp, which corresponds to a quantum yield of about 0.65 ×10^-3 at 260 mμ.     

THE WAVELENGTH DEPENDENCE OF HERPES SIMPLEX VIRUS INACTIVATION BY ULTRAVIOLET RADIATION

The effect of different wavelengths of ultraviolet (UV) radiation on Herpes simplex virus when assayed on mammalian cells (measured by plaque forming ability) was investigated. The wavelength dependence of viral inactivation was obtained for 11 different wavelengths over the region 238–297 nm. The resulting action spectrum does not closely follow the absorption spectrum of either nucleic acid or protein. The most effective wavelengths for viral inactivation are over the region 260–280 nm.     

INACTIVATION OF WILD-TYPE AND rad MUTANT Caenorhabditis elegans BY 8-METHOXYPSORALEN AND NEAR ULTRAVIOLET RADIATION

Survival of wild-type and four radiation-sensitive (rad) mutants of the nematode Caenorhabditis elegans was determined after near-UV irradiation in the presence of 8-methoxypsoralen (8-MOP). Three sets of inactivation profiles were generated for each strain by irradiating synchronous populations of either early embryos, late embryos or first-stage larvae (L1s). Late embryos were consistently the most sensitive. Curiously, none of the four rad mutants were even moderately hypersensitive. Split-dose experiments indicated that DNA-DNA crosslinks were primarily responsible for lethality. Crosslink induction and repair were determined using two different assays. In both cases, little if any repair was observed in wild-type. This lack of repair thus explains why the rad mutants were not hypersensitive to 8-MOP photoinactivation. Since early embryos undergo extensive cell cycling, their resistance to 8-MOP photoinactivation suggests that replication is highly refractory to both monoadducts and crosslinks, as has been demonstrated previously for UV radiation-induced photoproducts (Hartman et al., 1991, Mutat. Res., 255, pp. 163-173).     

ULTRAVIOLET ENHANCED REACTIVATION OF HERPES SIMPLEX VIRUS INACTIVATED BY DIFFERENT WAVELENGTHS OF UV RADIATION

The degree of ultraviolet enhanced reactivation (UVR) exhibited by mammalian cells when infected with Herpes simplex virus inactivated by different wavelengths of far ultraviolet (UV) radiation was measured. A wavelength dependence for this effect is presented over the wavelength region 238–297 nm. Within the limits of the deviations obtained, the degree of UVR exhibited is similar at each wavelength. This suggests that virus irradiated with different wavelengths of UV radiation received the same type of damage or that cells repaired the different types of viral damage with the same efficiency.     

聚丙烯膜表面光接枝聚合

对聚合物表面进行接枝聚合是一种有效的材料改性方法。近年来,S.Tazuke,Y.Ogiwara,高志民等人做了一些用紫外光引发接枝方面的工作,获得了较满意的结果。为提高聚丙烯(简称为PP)膜的光稳定性,我们研究了将一种受阻胺类光稳定剂,甲基丙烯酸2,2,6,6-四甲基哌啶醇酯(简称为MTMP)光接枝到PP膜表面的聚合过程。     

INACTIVATION OF PHAGE BY NEAR-ULTRAVIOLET RADIATION AND HYDROGEN PEROXIDE

A series of phage with different genomes (both single-stranded and double-stranded RNA and DNA) was inactivated with hydrogen peroxide (H₂O₂) in various combinations with far-ultraviolet (FUV) and near-ultraviolet (NUV) radiations. In every case but one (a lipid-coated phage), a sublethal H₂O₂ concentration greatly enhanced killing by NUV but not FUV. Moreover, this NUV/H₂O₂ synergism was oxygen independent and there was little if any host cell reactivation upon NUV plus H₂O₂ inactivation. These results suggest that these phage are inactivated by a common mechanism irrespective of nucleic acid composition, but that some phage genomes may be more vulnerable to NUV/H₂O₂ inactivation than others.     

PROTEIN ENHANCED INACTIVATION OF VIRAL DNA BY UV RADIATION

Abstract Viral DNA was irradiated in the presence of proteins and assayed for loss of biological activity. Several proteins were found to enhance the inactivation of transfecting ability by UV radiation. The sensitization caused by a particular protein depends upon its amino acid composition. Experiments done at low molar ratios of protein to DNA indicate that a protein-induced lesion could be a highly efficient means of inactivation.     

INACTIVATION OF THE LACTOSE PERMEASE OF ESCHERICHIA COLI BY MONOCHROMATIC ULTRAVIOLET LIGHT

Abstract— The lactose permease of E. coli is inactivated exponentially by seven wavelengths of monochromatic UV light. An action spectrum reveals that the shorter wavelengths (243, 290 and 313 nm) are much more efficient than longer wavelengths. Inactivation at 290 nm is most efficient and is not due to generalized membrane damage. The rate of counterflux of intracellular β-galactoside in response to externally added β-galactoside was slowed by 290 nm irradiation, indicating destruction of the facilitated diffusion mechanism. The induction of β-galactosidase and β-galactoside permease was co-ordinate both with and without pre-irradiation by 290 nm light. The β-galactosidase is approximately 26-fold more resistant to 290 nm than the permease. These results are discussed in terms of a greater sensitivity of membrane proteins to 290 nm light, which may be due to the role of aromatic amino acids in conferring stability to the permease in the membrane.     

A CLIMATOLOGY OF SUNBURNING ULTRAVIOLET RADIATION

Abstract— Data are presented from 14 sites where continuous measurements of the sun's shortest ultraviolet radiation reaching the earth's surface have been made for four or more years. Average daily dose per month and its variability from year to year is shown for each station. Some of the many influences affecting these measurements can be discerned by station intercomparisons. No consistent long term change in solar UV-B radiation reaching the ground is evident.     

INACTIVATION OF LIPID-CONTAINING VIRUSES BY HYDROPHOBIC PHOTOSENSITIZERS AND NEAR-ULTRAVIOLET RADIATION

Abstract—The hydrophobic photosensitizers acridine and phenothiazine inactivate the lipid-contnining viruses PM2,φ6, and herpes simplex when samples are illuminated with near-UV radiation. φ23–1- a . which is insensitive to organic solvents and presumably contains no lipids. is not inactivated under comparable conditions. For acridinc, the inactivation of virus requires that oxygen be present and is inhibited by sodium azide, implicating the involvement of singlet oxygen. For phenothiazine, oxygen is not required for photosensitized inactivation. Treatment of PM2 with acridine and near-UV light caused a complete disruption of the virion, as determined by sucrose gradient analysis of treated and untreated samples. These data and related observations suggest that lipid-containing viruses are inactivated through photosensitized membrane damage.     

THE DOSE-RESPONSE RELATIONSHIP OF TUMORIGENESIS BY ULTRAVIOLET RADIATION OF 254 nm

Abstract— Groups of albino hairless mice, Skh-hrl, were exposed daily to UVC radiation from low pressure Hg arcs (Philips TUV 40W). These lamps emit predominantly radiation of 254 nm. Three groups of animals were used in the experiments, each receiving a different daily dose.
The results were described with the Weibull probability function. As in earlier studies with UVB. the tumor induction time was proportional to a power of the daily dose. The exponent turned out to be as low as -0.2. This implies that the induction time varied only a little with the daily dose. The average number of tumors per animal was proportional to a power of time. A sample of 73 tumors of at least 4 mm in diameter were investigated histologically. The large majority were classified as squamous cell carcinomas.
A comparison was made with the results of an earlier reported experiment with Westinghouse FS40 sunlamps. Throughout the whole range of daily doses used in the present experiment, UVC was less carcinogenic than UVB. An intriguing difference between the two types of radiation was that the tumors induced by UVC appeared much more scattered over the irradiated parts of the animals than the UVB-induced tumors.     

ANGIOTENSIN ALTERATIONS INDUCED BY ULTRAVIOLET RADIATION*

Abstract. Angiotensin is readily inactivated by ultraviolet light presumably due to the photosensitivity of its tyrosyl and phenylalanyl residues. Alkalinity promotes and acidity delays the biological decomposition. Under conditions of oxygen exclusion (i.e. under N₂ or H₂) the rate of decomposition is further depressed and when irradiation is carried out under hydrogen a biologically active product is formed. This altered angiotensin, judging from its chromatographic migration and dialysis rate, represents a polymerized form of angiotensin. Under identical irradiation conditions, angiotensin was coupled with C¹⁴ labelled pheny-lalanine which indicates that this residue might be the photoreactive species. The production of altered forms of angiotensin by ultraviolet irradiation was discussed with respect to possible utility in anti-metabolite, antigen or tracer work.     

INHIBITION OF PROTEIN SYNTHESIS IN CULTURED TOBACCO CELLS BY ULTRAVIOLET RADIATION

Abstract— Ultraviolet (254 nm) irradiation of liquid-cultured tobacco cells strongly and quickly inhibited their ability to incorporate labeled amino acids into protein. An incident dose of only 388 J/m² reduced incorporation to 37 per cent of the original rate. The effect on amino acid incorporation did not seem to depend on inhibition of amino acid uptake, inhibition of the supply of nucleoside triphosphates, or inhibition of the supply of messenger RNA to cytoplasmic ribosomes.     

FORMATION OF THYMINE DIMERS IN MAMMALIAN SKIN BY ULTRAVIOLET RADIATION IN VIVO

Abstract— Ultraviolet radiation of 220–300 nm is known to produce cyclobutyl pyrimidine dimers in extracellular DNA, in bacteria, and in mammalian cells in culture. The formation in vivo of such dimers in mammalian skin has remained inferential. We report that one of the important and recognizable biologic events that occurs in mammalian skin during irradiation is the formation of thymine dimers. [³H]-labelled thymidine was applied to the epilated skin of guinea pigs to label their DNA. Animals were irradiated individually, using wavelengths of either 254, 285–350, or 320–400 nm. Immediately after irradiation, epidermis was separated from the rest of the skin and homogenized; DNA and RNA were isolated. Irradiation with wavelengths of 285–350 nm, which included the sunburn-producing spectrum (i.e., 290–320 nm), produced thymine dimers (1·7–2·6 per cent of the total [³H]-thymine incorporated into DNA). Irradiation with 254nm also produced fewer dimers (0·46–1·2 percent); and 320–400 nm produced none. The dimer could be cleaved by 250 nm radiation to form thymine. The epidermal cell damage by ultraviolet radiation, particularly by the sunburn-producing spectrum (290–320 nm), may be related to the formation of such dimers.     

INDUCTION OF PHOTOPRODUCTS IN SYNTHETIC POLYNUCLEOTIDES BY FAR AND NEAR ULTRAVIOLET RADIATION

Single and double-stranded polynucleotides of thymine and cytosine have been used to analyse the photoproducts produced by irradiation with far or near UV light. Reversed-phase high performance liquid chromatography was used to detect and quantify cyclobutane dimers and Pyr(6–4)Pyo adducts produced by 254 nm. At 320 nm 10-times less Thy(5–6)Thy dimers and one half the number of Cyt(5–6)Cyt dimers were induced; no Pyr(6–4)Pyo adducts were evident. HPLC has recently been applied to the isolation and characterization of various nucleic acid substituents and their UV-photoproducts. The relative retention times of pyrimidines and their UV photoproducts on HPLC reflect differences in the hydrophobicity of the compounds being separated. Hence, the more hydrophobic (less polar) a compound is, the greater its capacity to bind to the column and the greater its retention time; for T o T, C<>T and C<>C dimers this difference may result from variations in the number of methyl moieties (Cadet et al., 1983). The retention time of the compound also depends on its stereochemistry. Separation of the four stereoisomers of T<>T by HPLC shows that compounds which are molecular equivalents can be more or less accessible to the non-polar stationary phase depending on their conformation (Cadet, 1980). The relatively long retention times of the bipyrimidine photoadducts suggest a structural configuration which allows greater access to the hydrophobic moieties of the molecule. It is intriguing to consider that this difference in conformation may also be reflected in DNA–protein interactions such as binding by UV-endonucleases or antibodies directed against UV photodamage. Proteins can be used as sensitive probes for photoproduct induction and repair but an accurate evaluation of their specificity is required. It was the intent of this paper not only to compare the induction parameters for various dimers in pyrimidine homo-polymers but to provide controlled substrates which can be used to define the relative binding efficiencies of repair enzymes and antibodies for different types of photoproducts.     

MOLECULAR MECHANISMS OF ULTRAVIOLET RADIATION CARCINOGENESIS

UV radiation is a potent DNA damaging agent and a known inducer of skin cancer in experimental animals. There is excellent scientific evidence to indicate that most non-melanoma human skin cancers are induced by repeated exposure to sunlight. UV radiation is unique in that it induces DNA damage that differs from the lesions induced by any other carcinogen. The prevalence of skin cancer on sun-exposed body sites in individuals with the inherited disorder XP suggests that defective repair of UV-induced DNA damage can lead to cancer induction. Carcinogenesis in the skin, as elsewhere, is a multistep process in which a series of genetic and epigenetic events leads to the emergence of a clone of cells that have escaped normal growth control mechanisms. The principal candidates that are involved in these events are oncogenes and tumor suppressor genes. Oncogenes display a positive effect on transformation, whereas tumor suppressor genes have an essentially negative effect, blocking transformation. Activated ras oncogenes have been identified in human skin cancers. In most cases, the mutations in the ras oncogenes have been localized to pyrimidine-rich sequences, which indicates that these sites are probably the targets for UV-induced DNA damage and subsequent mutation and transformation. The finding that activation of ras oncogenes in benign and self-regressing keratoacanthomas in both humans and in animals indicates that they play a role in the early stages of carcinogenesis (Corominas et al., 1989; Kumar et al., 1990). Since cancers do not arise immediately after exposure to physical or chemical carcinogens, ras oncogenes must remain latent for long periods of time. Tumor growth and progression into the more malignant stages may require additional events involving activation of other oncogenes or deletion of growth suppressor genes. In addition, amplification of proto-oncogenes or other genes may also be involved in tumor induction or progression. In contrast to the few studies that implicate the involvement of oncogenes in UV carcinogenesis, the role of tumor suppressor genes in UV carcinogenesis is unknown. Since cancer-prone individuals, particularly XP patients, lack one or more repair pathways, one can speculate that DNA repair enzymes would confer susceptibility to both spontaneous and environmentally induced cancers. Another potential candidate that can function as a tumor suppressor gene is the normal c-Ha-ras gene. Spandidos and Wilkie (1988) have shown that the normal c-Ha-ras gene can suppress transformation induced by the mutated ras gene.(ABSTRACT TRUNCATED AT 400 WORDS)