Abstract:Abstract— –The induction of mutation to phage T5 resistance by near ultraviolet (u.v.) and visible light was studied in chemostat cultures of Escherichia coli strains B/r and B/r/1, trp. The visible light mutation rate to phage T5 resistance was independent of growth rate over the range studied. This result is consistent with a photochemical mechanism of mutagenesis. Changeovers, in which a faster growing subpopulation takes over the culture, usually causing the mutant frequency to decline sharply, occur more … Show more
“…Most of these individuals are also defective in excision repair (17,18), and the severity of the disease is related to the magnitude of the defect (18). They are the analogs of UV-sensitive bacteria and we argue by analogy to bacteria that damage to DNA is the important photochemical damage to human cells, and thus make the (20,21) (0, *), mutations in E. coli (22) (A), killing T4 and T6 phages (23,24) (@, 0), photoproducts in DNA (25) The dotted curve is a recent erythemal action spectrum (29). strong inference that damage to DNA that is not repaired effectively results in mutation and the transformation of cells.…”
DNA is taken as the target for skin cancer induced by ultraviolet light, and the known data on the sensitivity of DNA as a function of wavelength are summarized. The sun's spectrum at the surface of the earth and the DNA action spectrum are used to calculate the carcinogenic effectiveness as a function of wavelength.The most effective wavelengths at 30'N latitude are <305 nm, and a 1% change in atmospheric ozone results in a 2% change in the effective dose of ultraviolet light. Since both the basic biological and physical data are reasonably precise, the major requirement for a quantitative evaluation of the dose response relation for ultraviolet-induced skin cancer in man is better epidemiological data to compare with data from animal models.Human skin cancers, especially basal and squamous cell carcinomas, are closely associated with exposure to sunlight.[See reviews by Blum (1), Epstein (2), and the volume edited by Urbach (3). ] Three lines of evidence indicate that the most effective wavelengths are below 320 nm. (i) In mice, wavelengths longer than 320 nm are ineffective in inducing skin cancer although a recent report indicates that exposure to the longer wavelengths may accentuate the effects of shorter ones (4). (ii) The effective wavelengths for erythema production are below 320 nm. Skin cancer and erythema arise in the same tissue, and individuals who sunburn easily have a higher probability than average of developing skin cancer (5, 6). (iii) Ultraviolet light (UV)-induced skin cancer probably arises from photochemical changes in DNA, and the shorter wavelengths are much more effective than. the longer ones in damaging this polymer (see below). Interest in wavelength dependence arises not only because of the inherent interest in the problem but also for the practical reason of estimating the effects of this model environmental hazard. The hazard could change. For example, the exhausts from a fleet of supersonic transports might result in a decrease in stratospheric -ozone and the attendant increase in UV fluence at the earth's surface could result in an increase in the incidence rate of skin cancer. This particular problem has been succinctly stated (7). If we are to evaluate quantitatively such hazards, we must have good animal and epidemiological data as well as a theoretical framework to handle such data.UV-induced skin cancer deserves more careful epidemiological study because (i) we know more about UV-induced lesions in DNA than any other physicochemical insult to the Abbreviation: UV, ultraviolet light.
“…Most of these individuals are also defective in excision repair (17,18), and the severity of the disease is related to the magnitude of the defect (18). They are the analogs of UV-sensitive bacteria and we argue by analogy to bacteria that damage to DNA is the important photochemical damage to human cells, and thus make the (20,21) (0, *), mutations in E. coli (22) (A), killing T4 and T6 phages (23,24) (@, 0), photoproducts in DNA (25) The dotted curve is a recent erythemal action spectrum (29). strong inference that damage to DNA that is not repaired effectively results in mutation and the transformation of cells.…”
DNA is taken as the target for skin cancer induced by ultraviolet light, and the known data on the sensitivity of DNA as a function of wavelength are summarized. The sun's spectrum at the surface of the earth and the DNA action spectrum are used to calculate the carcinogenic effectiveness as a function of wavelength.The most effective wavelengths at 30'N latitude are <305 nm, and a 1% change in atmospheric ozone results in a 2% change in the effective dose of ultraviolet light. Since both the basic biological and physical data are reasonably precise, the major requirement for a quantitative evaluation of the dose response relation for ultraviolet-induced skin cancer in man is better epidemiological data to compare with data from animal models.Human skin cancers, especially basal and squamous cell carcinomas, are closely associated with exposure to sunlight.[See reviews by Blum (1), Epstein (2), and the volume edited by Urbach (3). ] Three lines of evidence indicate that the most effective wavelengths are below 320 nm. (i) In mice, wavelengths longer than 320 nm are ineffective in inducing skin cancer although a recent report indicates that exposure to the longer wavelengths may accentuate the effects of shorter ones (4). (ii) The effective wavelengths for erythema production are below 320 nm. Skin cancer and erythema arise in the same tissue, and individuals who sunburn easily have a higher probability than average of developing skin cancer (5, 6). (iii) Ultraviolet light (UV)-induced skin cancer probably arises from photochemical changes in DNA, and the shorter wavelengths are much more effective than. the longer ones in damaging this polymer (see below). Interest in wavelength dependence arises not only because of the inherent interest in the problem but also for the practical reason of estimating the effects of this model environmental hazard. The hazard could change. For example, the exhausts from a fleet of supersonic transports might result in a decrease in stratospheric -ozone and the attendant increase in UV fluence at the earth's surface could result in an increase in the incidence rate of skin cancer. This particular problem has been succinctly stated (7). If we are to evaluate quantitatively such hazards, we must have good animal and epidemiological data as well as a theoretical framework to handle such data.UV-induced skin cancer deserves more careful epidemiological study because (i) we know more about UV-induced lesions in DNA than any other physicochemical insult to the Abbreviation: UV, ultraviolet light.
“…Other DNA photoproducts are induced by near ultraviolet and visible light through photodynamic action, a mechanism involving the interaction of light with certain fluorescent, cellular components (24). Such damage has been implicated in bacterial mutagenesis (25,26) and could also be a causal agent in transformation by fluorescent light. In addition, DNA strand breaks (6) and DNA cross-links (7) are induced by fluorescent light.…”
Aftershocks of the 29 November 1978 Oaxaca, Mexico, earthquake (surface-wave magnitude Ms = 7.8) define a rupture area of about 6000 square kilometers along the boundary of the Cocos sea-plate subduction. This area had not ruptured in a large (Ms >/= 7), shallow earthquake since the years 1928 and 1931 and had been designated a seismic "gap." The region has also been seismically quiet for small to moderate (M >/= 4), shallow (depth = 60 kilometers) earthquakes since 1966; this quiet zone became about six times larger in 1973. A major earthquake (Ms = 7.5 +/- 0.25) was forecast at this location on the basis of the quiescence that began in 1973. The aftershock data indicate that an area approximately equivalent in size to the seismic gap has now broken.
“…Dr. Webb (Argonne National Laboratory) then reviewed the discovery of mutation due to near UV and showed apparatus which could be used for the study of continuous development of mutations (Webb and Kubitschek, 1964; Webb and Malina, 1970). The work he presented was primarily on mutations of E. coli B/r to resistance to phage T5 and to streptomycin.…”
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