Oygen Dependence and Repair of Lethal Effects of Near Ultraviolet and Visible Light*

Webb, Robert B.; Lorenz, John R.

doi:10.1111/j.1751-1097.1970.tb06060.x

Cited by 107 publications

(42 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Webb and Lorenz (19) reported a temperaturesensitive, oxygen-dependent system in E. coli which repairs damage induced by broad-spectrum visible light (390-740 nm). The presence of a shoulder on killing curves might also be due to a multihit process or to cell clumping, but examination of wet mounts after cells were exposed to light did not reveal greater clumping of DPA-grown cells than of control cells.…”

Section: Resultsmentioning

confidence: 99%

Action of light on Micrococcus roseus

Schwartzel¹,

Cooney²

1974

Can. J. Microbiol.

View full text Add to dashboard Cite

1974. Action of light on Micrococc~ts roseus. Can. J.Microbiol. 20: 1015-1021. Micrococc~ts roseus is killed by exposure to a continuous spectrum of white light (3000 ft-c (32 292 Im/m2)) in the presence of air and the dye, toluidine blue. Comparison of rates of photodynamic killing for log and stationary phase cells and for two pigmentation mutants indicated that photosensitivity could not be correlated with amount of carotenoid or with carotenoid-chromophore length. Moreover, cells grown in medium containing diphenylamine (DPA) did not contain significant quantities of colored carotenoids; they were not as sensitive to photodynamic killing as fully pigmented cclls. Photodynamic killing was accompanied by selective release of magnesium and calcium and by release of UV-absorbing material. In the absence of added photosensitizer, M. rosetts, the two mutants, or DPA-inhibited cells were not killed when exposed to white light at intensities as high as 22 000 ft-c (236 806 Im/m2) for a s long as 9 h, and cells did not release UV-absorbing material. Under these conditions M . roseus and the yellow mutant did not release as much magnesium or calcium as when subjected to photodynamic killing, but DPA-grown cells leaked sodium, magnesium, and calcium. These observations are consistent with several suggestions: (i) carotenoids do not serve as photochemical buffers in M. roserts; (ii) growth in medium containing DPA or mutations leading to altered pigmentation change membrane organization leading to altered photosensitivity; (iii) M. roseus has an efficient repair mechanism which renders it resistant to photodynamic killing unless an exogenous photosensitizer is present. SCHWARTZEL, E. H., et J. J. COONEY. 1974. Action of light on Micrococcus roseus. Can. J.Microbiol. 20: 1015-1021. Micrococcus roselts est tuC par I'exposition un spectre continu de lumiere blanche (3000 ft-c (32 292 Im/m2)) en presence de I'air et d'un colorant toluidine bleu. La comparaison des taux de mortalite photodynamique pour les cellules en phase logarithmique et en phase stationnaire et pour les deux mutants a la pigmentation indique que la photosensibilite ne peut pas &tre corrdee avec la quantitt de carotkno'ide ou avec la longueur du chromophore caroteno'ide. En plus, les cellules qui se sont developpees dans un milieu contenant la diphenylamine (DPA) ne contiennent pas de quantitt significative de carotenoi'des colorees; elles ne sont pas aussi sensibles a la mortalit6 photodynamique que les cellules entierement pigmentees. La mortalit6 photodynamique est accompagnke par une liberation selective du magntsium et du calcium e t de materiel absorbant I'UV. En I'absence de photosensibilisateurs, M . roseus, les deux mutants, ou lcs cellules inhibks au DPA, ne sont pas tuees lorsqu'elles sont exposees a la lumitre blanche a des intensites aussi hautes que 22 000 ft-c (236 806 Im/m2) pour aussi longtemps que 9 1.1, et les cellules ne liberent pas de materiel absorbant I'UV. Sous ces conditions, M . rosetts et le mutant jaune ne liberent pas autant d...

show abstract

Section: Resultsmentioning

confidence: 99%

Action of light on Micrococcus roseus

Schwartzel¹,

Cooney²

1974

Can. J. Microbiol.

View full text Add to dashboard Cite

show abstract

“…The relative importance of DNA and membrane damage in the lethal and sublethal actions of NUV light on E. coli are still unclear. In the early seventies it was demonstrated that NUV inactivation is oxygen-dependent (Eisenstark, 1970;Webb and Lorenz, 1970). This finding was followed by many studies showing that NUV light produces reactive oxygen species (ROS) via sensitization of endogenous photosensitizers (e.g.…”

Section: Introductionmentioning

confidence: 99%

Gene expression of Escherichia coli in continuous culture during adaptation to artificial sunlight

Berney¹,

Weilenmann²,

Egli³

2006

Environmental Microbiology

View full text Add to dashboard Cite

Escherichia coli growing in continuous culture under continuous UVA irradiation exhibits growth inhibition with a subsequent adaptation to the stress. Transcriptome analysis was performed during transient growth inhibition and in the UVA light-adapted growth state. The results indicate that UVA light induces stringent response and an additional response that includes the upregulation of the synthesis of valine, isoleucine, leucine, phenylalanine, histidine and glutamate. The induction of several SOS response-genes strongly points to DNA damage as a result of UVA exposure. The involvement of oxidative stress was observed with the induction of ahpCF. Taken together it supports the hypothesis of the production of reactive oxygen species by UVA light. In the UVA-adapted cell population strong repression of the acid tolerance response was found. We identified the enzyme chorismate mutase as a possible chromophore for UVA light-inactivation and found strong repression of the pyrBI operon and the gene mgtA encoding for an ATP-dependent Mg2+ transporter. Furthermore, our results indicate that the role of RpoS may not be as important in the adaptation of E. coli to UVA light as it was implicated by previous results with starved cells, but that RpoS might be of crucial importance for the resistance under transient light exposure.

show abstract

“…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.…”

Section: Carcinogenic Action Spectrummentioning

confidence: 99%

The Wavelengths in Sunlight Effective in Producing Skin Cancer: A Theoretical Analysis

Setlow

1974

Proc. Natl. Acad. Sci. U.S.A.

1,063

618

View full text Add to dashboard Cite

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.

show abstract

Oygen Dependence and Repair of Lethal Effects of Near Ultraviolet and Visible Light*

Cited by 107 publications

References 8 publications

Action of light on Micrococcus roseus

Action of light on Micrococcus roseus

Gene expression of Escherichia coli in continuous culture during adaptation to artificial sunlight

The Wavelengths in Sunlight Effective in Producing Skin Cancer: A Theoretical Analysis

Contact Info

Product

Resources

About