Lethal Effects of Natural Solar Ultraviolet Radiation in Repair Proficient and Repair Deficient Strains of Escherichia Coli: Actions and Interactions

Tyrrell, Rex M.; Souza-Neto, A.

doi:10.1111/j.1751-1097.1981.tb09005.x

Cited by 9 publications

(17 citation statements)

References 13 publications

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“…2 of the present manuscript and in Ref. 15). From the linear portion of the inactivation curves, it can be calculated that it took 24 min of noon sunlight in Rio de Janeiro at the summer solstice to inactivate one Log 10 of (strain AB1157) E. coli (obtained from Ref.…”

Section: Discussionsupporting

confidence: 58%

“…The time around solar noon that we found was needed to reduce the bacterial load of P. aeruginosa by 4 Log 10 was 39 min (9.7 min per Log 10 ) on June 29 near Hamburg, Germany (53°0′N latitude). This inactivation rate obtained a few days after the summer solstice was compared with previous experiments exposing a repair-proficient control strain (K12 AB 1157) of E. coli in Rio de Janeiro (22°54′S latitude) during December 21, 1978 which is the summer solstice in the Southern hemisphere (15). The patterns of solar inactivation kinetics of P. aeruginosa presented here and of E. coli AB 1157 previously reported were similar with both inactivation curves showing a shoulder region followed by a relatively rapid linear decay (comparing data in Fig.…”

Section: Discussionmentioning

confidence: 85%

“…Sunlight radiation is the main environmental germicide, but few studies have investigated the effect of solar ultraviolet (UV) radiation on bacteria that can persist in varied environments and cause human disease. Experimental data on the inactivation of Bacillus spores (14), of repair-deficient and -proficient mutant strains of Escherichia coli (15), and of Burkholderia pseudomallei (16) by sunlight has been reported previously. The objective of this study was to determine the inactivation rate of P. aeruginosa exposed to sunlight, to gain an insight about the ability of this organism to survive in the environment from where it can disperse and cause disease to humans.…”

Section: Introductionmentioning

confidence: 99%

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Inactivation of Pseudomonas aeruginosa by Direct Sunlight

Sagripanti¹,

Grote

Niederwöhrmeier

et al. 2013

Photochem & Photobiology

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We determined the sensitivity of Pseudomonas aeruginosa to direct sunlight radiation, while maintaining the experimental temperature below levels harmful to the bacterium. The results presented here were similar to previous data on solar sensitivity obtained half a world away on another related bacterial species. The findings presented in this study suggest that related bacteria have a characteristic sensitivity to sunlight with their survival depending mainly on the fluence (photons) received in a dose-dependent manner that is otherwise relatively independent from latitude, atmospheric ozone and other local conditions. Conditions that inactivated P. aeruginosa did not result in measurable impairment of specific polymerase chain reaction (PCR) or enzyme-linked immunoassays (ELISA) tests suggesting that this germ could still be amenable to detection after inactivation by sunlight. The results presented in this study should assist in predicting the survival of P. aeruginosa outdoors and in monitoring the risk posed by this widespread organism in a variety of environmental settings.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

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Inactivation of Pseudomonas aeruginosa by Direct Sunlight

Sagripanti¹,

Grote

Niederwöhrmeier

et al. 2013

Photochem & Photobiology

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“…Multiple sublethal exposures to solar UV radiation may occur before the cells divide. Previous studies with bacteria (29,30) allow the estimate that '15 min of noon winter sunlight (Rio de Janeiro, sea level) will produce DNA damage equivalent to that of about 3 J.m-2 of UV at a wavelength of 254 nm. Even though penetration of solar UV (290-320 nm) into the upper dermis is only a few percent of that reaching the skin's surface (31), fibroblasts in this region would accumulate UV damage of the order described in these studies within a few hours of sunlight exposure.…”

Section: Discussionmentioning

confidence: 99%

Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.

Tyrrell¹

1984

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

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Nondividing (arrested) populations of primary human fibroblasts from normal individuals exposed to an initial dose (1.5 or 3 J m-2) of far-UV (254 nm) radiation and then incubated in medium containing low (0.5%) serum develop enhanced resistance to inactivation of cloning efficiency by a second (challenge) dose of UV. The resistance develops within 2-4 days, after which there is a decline. Resistance develops to a higher degree and more rapidly (1-2 days) in cells derived from patients with the variant form of xeroderma pigmentosum. Excision-deficient cells from xeroderma pigmentosum complementation group A individuals also develop UV resistance after a lower (0.2 J m-2) exposure to UV. Enhanced UV resistance does not develop in UV-irradiated cell populations incubated with the protein synthesis inhibitor cycloheximide (5 IPM). These observations are consistent with the interpretation that exposure of human fibroblasts to low doses of UV induces synthesis of a protein involved in a metabolic pathway that transiently enhances the capacity of cells to repair potentially lethal damage resulting from a subsequent dose of UV.The genetic control and biochemistry of an error-prone far-UV inducible repair system in Escherichia coli has been extensively studied (see ref. 1 for overview). Recent experiments have begun to clarify the nature of the inducing signal (2) and enzymology (3) of the process. The existence of a similar phenomenon in eukaryotic cells has been largely inferred from viral reactivation studies (4). The survival of many types of UV-damaged virus is enhanced by pre-exposure of the appropriate host cells to UV radiation and incubation for an appropriate time prior to viral infection (see ref.5 for review). The nature and degree of error-proneness of the response, as deduced from enhanced mutagenesis of infecting virus (6, 7), appears to vary considerably with the particular virus and host cell system employed. For example, the mutability of intact but not UV-irradiated parvovirus H1 is enhanced in UV pretreated human or rat cells (8), whereas only enhanced mutability of UV-treated virus is seen when simian virus 40 infects UV-treated monkey cells (7). Findings opposite to the latter have been reported (9, 10).Biochemical measurements of UV-induced responses in mammalian cells have been controversial. A report of enhancement of post-replication repair by a low-dose UV-conditioning exposure (11) may also be interpreted (12) on the basis of the abnormal state of DNA replication at the time of the second exposure. Nevertheless, UV exposure of human fibroblasts has been shown to enhance levels of plasminogen activator (13) and DNA ligase (14), and agents that arrest DNA replication have been shown recently to induce synthesis of a nuclear membrane-bound protein in cell lines derived from B lymphocytes (15).Little is known about whether UV treatment actually enhances the capacity of mammalian cells to survive subsequent challenge doses of UV. Split-dose experiments are often difficult to interpret (16)...

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“…A recent application using a DNA repair-deficient Escherichia coli strain to measure UV in Antarctica (1 1-14) demonstrated sufficient sensitivity to detect UVB up to 25 m deep in Antarctic waters during the presence of an ozone "hole." Biological organisms, such as E. coli (11,15,16), bacteriophage TI, T2 and T7 (17)(18)(19), spores of Bacillus subtilis, both repair-deficient and wildtype strains (20)(21)(22)(23)(24), have some drawbacks in their application. First, different organisms with different repair capacities (12) confound comparisons.…”

Section: Introductionmentioning

confidence: 99%

UVB DNA Dosimeters Analyzed by Polymerase Chain Reactions

Yoshida

Regan

1997

Photochem & Photobiology

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Purified bacteriophage lambda DNA was dried on a UV-transparent polymer film and served as a UVB dosimeter for personal and ecological applications. Bacteriophage lambda DNA was chosen because it is commercially available and inexpensive, and its entire sequence is known. Each dosimeter contained two sets of DNA sandwiched between UV-transparent polymer films, one exposed to solar radiation (experimental) and another protected from UV radiation by black paper (control). The DNA dosimeter was then analyzed by a polymerase chain reaction (PCR) that amplifies a 500 base pair specific region of lambda DNA. Photoinduced damage in DNA blocks polymerase from synthesizing a new strand; therefore, the amount of amplified product in UV-exposed DNA was reduced from that found in control DNA. The average lesion frequency per 500 base pair per strand at 16 PCR cycles was approximately 1.22, 1.00, 0.70 and 0.50 for 30 ng, 50 ng, 100 ng and 150 ng of dried DNA, respectively, after a total dose of 60 kJ m(-2) delivered with a solar UVB simulator. Although the average lesion frequency increases linearly with increasing doses for four different amounts of template DNA, the lesion frequency seems to be averaged by the amplified products from the protected lambda DNA molecules below the top few layers. The average daily dose, equivalent to the UV dose applied with the solar UVB simulator was 10.2 +/- 0.4 kJ m(-2) with the 50 ng containing DNA dosimeter in September 1995 in Melbourne, FL. Both 50 ng and 150 ng containing DNA dosimeters produced the same average daily dose within experimental error in January 1996, which was 5.2 +/- 0.3 kJ m(-2) at the same location. The dried lambda DNA dosimeter is compact, robust, safe and transportable, stable over long storage times and provides the total UVB dose integrated over the exposure time.

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Lethal Effects of Natural Solar Ultraviolet Radiation in Repair Proficient and Repair Deficient Strains of Escherichia Coli: Actions and Interactions

Cited by 9 publications

References 13 publications

Inactivation of Pseudomonas aeruginosa by Direct Sunlight

Inactivation of Pseudomonas aeruginosa by Direct Sunlight

Exposure of nondividing populations of primary human fibroblasts to UV (254 nm) radiation induces a transient enhancement in capacity to repair potentially lethal cellular damage.

UVB DNA Dosimeters Analyzed by Polymerase Chain Reactions

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