Enhancement of Photorepair of Ultraviolet‐induced Pyrimidine Dimers by Preillumination With Fluorescent Light in the Goldfish Cell Line. The Relationship Between Survival and Yield of Pyrimidine Dimers

Yasuhira, Shinji; Mikami, Hiroshi; Shima, Akihiro

doi:10.1111/j.1751-1097.1992.tb04214.x

Cited by 29 publications

(10 citation statements)

References 25 publications

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“…We show here that natural levels of solar UVB during ozone depletion may also cause measurable damage to multicellular organisms occupying higher trophic levels of the Antarctic marine ecosystem. The level of UVB-induced DNA damage measured in ichthyoplankton is greater than the lethal limit previously determined for Antarctic diatoms (Ͼ15 CPDs per Mb) and is comparable to the lethal limit of DNA damage for cultured goldfish cells (20-100 CPDs per Mb) (25,45). Despite substantial temporal changes in solar intensity, cloud cover, water column turbidity, and vertical mixing of the zooplankters during the sampling period, more than half of all specimens contained measurable DNA damage at levels that are probably physiologically relevant.…”

Section: Discussionmentioning

confidence: 54%

Solar UVB-induced DNA damage and photoenzymatic DNA repair in antarctic zooplankton

Malloy

Holman

Mitchell

et al. 1997

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

204

169

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The detrimental effects of elevated intensities of mid-UV radiation (UVB), a result of stratospheric ozone depletion during the austral spring, on the primary producers of the Antarctic marine ecosystem have been well documented. Here we report that natural populations of Antarctic zooplankton also sustain significant DNA damage [measured as cyclobutane pyrimidine dimers (CPDs)] during periods of increased UVB f lux. This is the first direct evidence that increased solar UVB may result in damage to marine organisms other than primary producers in Antarctica. The extent of DNA damage in pelagic icefish eggs correlated with daily incident UVB irradiance, ref lecting the difference between acquisition and repair of CPDs. Patterns of DNA damage in fish larvae did not correlate with daily UVB f lux, possibly due to different depth distributions and͞or different capacities for DNA repair. Clearance of CPDs by Antarctic fish and krill was mediated primarily by the photoenzymatic repair system. Although repair rates were large for all species evaluated, they were apparently inadequate to prevent the transient accumulation of substantial CPD burdens. The capacity for DNA repair in Antarctic organisms was highest in those species whose early life history stages occupy the water column during periods of ozone depletion (austral spring) and lowest in fish species whose eggs and larvae are abundant during winter. Although the potential reduction in fitness of Antarctic zooplankton resulting from DNA damage is unknown, we suggest that increased solar UV may reduce recruitment and adversely affect trophic transfer of productivity by affecting heterotrophic species as well as primary producers.

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Section: Discussionmentioning

confidence: 54%

Solar UVB-induced DNA damage and photoenzymatic DNA repair in antarctic zooplankton

Malloy

Holman

Mitchell

et al. 1997

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

204

169

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“…In cultured fish cells, dark repair (nucleotide excision repair, NER) has been suggested to proceed at a very slow rate relative to mammalian cells (Regan and Cook, 1967;Woodhead et al, 1980;Shima et al, 1981;Mano et al, 1982;Regan et al, 1982;Park and Li, 1989). In contrast, several reports indicate that fish cells possess robust photoenzymatic repair capabilities specific for both UV-induced pyrimidine dimers (PyP) and 6-4 photoproducts (6-4PD) (Yasuhira et al, 1992;Ahmed et al, 1993;Uchida et al, 1997Uchida et al, , 1998Meador et al, 2000;and Mitchell et al, this issue). In a recent report, intact fish were exposed to UV light, then DNA from their skin and fin was assayed at various times after exposure (Meador et al, 2000).…”

Section: Introductionmentioning

confidence: 87%

Relative Base Excision Repair in Xiphophorus Fish Tissue Extracts

Walter

Sung

Obermoeller

et al. 2001

Marine Biotechnology

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To begin characterizing DNA repair capability among Xiphophorus species, we adapted oligonucleotide-based DNA repair assays to extracts of fish tissues. Here, we report the initial results of relative base excision repair (BER) capability among 3 inbred Xiphophorus fish lines representing 2 species (X. maculatus and X. couchianus), and interspecies hybrid F(1) animals produced by crossing them. Overall, data from uracil- N-glycosylase (UNG)-initiated BER assay (UNG-BER) indicate that brain tissue extracts generally possess higher BER activity than do gill and liver extracts. UNG-BER activities in gill and liver extracts were similar. The BER activity in the tissues of F(1) interspecies hybrids followed the activity pattern of the X. couchianus parent in gill and liver extracts, was similar to the X. maculatus parent in brain extracts, but exhibited a reduced repair capacity in gill tissue extracts compared with either parent. We discuss the use of oligonucleotide-based DNA repair assays to elucidate the role that inheritance of DNA repair potential may play in susceptibility to disease and tumorigenesis in the intact organism.

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“…Negligible attenuation by the plastic chamber or water was observed. To prevent unwanted white light effects like lightinducible PER (33)(34)(35), fry were kept in the dark for 24 h before the first exposure until 24 h after the last exposure. Fig.…”

Section: Methodsmentioning

confidence: 99%

Ultraviolet A does not induce melanomas in a Xiphophorus hybrid fish model

Mitchell

Fernandez

Nairn

et al. 2010

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

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We examined the wavelength dependence of ultraviolet (UV) radiation (UVR)-induced melanoma in a Xiphophorus backcross hybrid model previously reported to be susceptible to melanoma induction by ultraviolet A (UVA) and visible light. Whereas ultraviolet B (UVB) irradiation of neonates yielded high frequencies of melanomas in pigmented fish, UVA irradiation resulted in melanoma frequencies that were not significantly different from unirradiated fish. Spontaneous and UV-induced melanoma frequencies correlated with the degree of pigmentation as expected from previous studies, and the histopathology phenotypes of the melanomas were not found in significantly different proportions in UV-treated and -untreated tumor-bearing fish. Our results support the conclusion that a brief early-life exposure to UVB radiation causes melanoma formation in this animal model. These data are consistent with an essential role for direct DNA damage, including cyclobutane dimers and (6-4) photoproducts, in the etiology of melanoma.ultraviolet B | DNA damage | cyclobutane dimer | reactive oxygen species | melanin I n the late 1980s Setlow and coworkers used genetic hybrids from interspecific crosses involving several species of the fish genus Xiphophorus to investigate the effects of UVR on the induction of cutaneous malignant melanoma (CMM) (1). These pioneering studies demonstrated that ultraviolet B (UVB) irradiation of backcross hybrids generated from a specific genetic crossing scheme induced melanomas at significant frequencies above spontaneous levels. These results were later confirmed, and the genetic basis of UVB-induced melanoma susceptibility in this cross was recognized to be the same as in the well-studied spontaneous Xiphophorus hybrid melanoma model (2). In 1993, Setlow used a different Xiphophorus interspecies cross (designated as Sp-couchianus; Fig. 1) to study the wavelength dependence of melanoma induction and reported that wavelengths in the ultraviolet A (UVA) and visible ranges were effective in inducing melanomas in first-generation backcross (BC 1 ) hybrids generated from this particular cross (3). An action spectrum for melanoma induction was proposed with maxima in the UVB (302/313 nm) and UVA (365 nm) ranges. Because UVA fluence is quantitatively much greater than UVB in sunlight incident to the earth's surface (∼10-fold), Setlow suggested that, on the basis of this action spectrum, UVA was more effective than UVB in causing melanomas in the human population (2, 4). This report had significant public health consequences; it suggested that the use of commercially available sunscreens that effectively blocked UVB but not UVA encouraged more lengthy recreational sunlight exposure and thereby increased the exposure to UVA and its associated risks. Over the past 20 years, these data have become central to the debate on the role of UVA in melanoma and the risks associated with recreational and artificial exposures to UVA wavelengths.Debate over the action spectrum for melanoma has only intensified because subsequent r...

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Enhancement of Photorepair of Ultraviolet‐induced Pyrimidine Dimers by Preillumination With Fluorescent Light in the Goldfish Cell Line. The Relationship Between Survival and Yield of Pyrimidine Dimers

Cited by 29 publications

References 25 publications

Solar UVB-induced DNA damage and photoenzymatic DNA repair in antarctic zooplankton

Solar UVB-induced DNA damage and photoenzymatic DNA repair in antarctic zooplankton

Relative Base Excision Repair in Xiphophorus Fish Tissue Extracts

Ultraviolet A does not induce melanomas in a Xiphophorus hybrid fish model

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