New trends in photobiology

Cadet, Jean; Anselmino, Catherine; Douki, Thierry; Voituriez, L.

doi:10.1016/1011-1344(92)85135-h

Cited by 193 publications

(46 citation statements)

References 106 publications

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“…The yields of CPD formed by UVC and UVB radiation shown in table 1 are in excellent agreement with those reported in the literature (33,(39)(40)(41)(42)(43). In addition, we observed induction of CPD by UVA radiation in mammalian cells ( figure 3).…”

Section: Cpd and Uva Radiation Role In Solar Mutagenesissupporting

confidence: 81%

“…This illustrates that the distribution of the different classes of photolesion varies depending on the UV source, as already observed (21,22,35), and clearly demonstrates that the biological effects of sunlight cannot be deduced solely on the basis of studies with UVC. Furthermore, DewarPP was formed with high yield, making it the third major photolesion induced by SSL (about ten times more frequent than 8-oxodGuo (15) or cytosine hydrates (43)). This indicates that this lesion may contribute in a previously unsuspected manner to the effects produced by sunlight exposure.…”

Section: Dewarpp a Major Lesion Induced By Sunlightmentioning

confidence: 99%

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Distribution and repair of bipyrimidine photoproducts in solar UV-irradiated mammalian cells. Possible role of Dewar photoproducts in solar mutagenesis

Perdiz

Gróf

Mezzina

et al. 2000

Journal of Biological Chemistry

146

177

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Section: Cpd and Uva Radiation Role In Solar Mutagenesissupporting

confidence: 81%

Section: Dewarpp a Major Lesion Induced By Sunlightmentioning

confidence: 99%

Distribution and repair of bipyrimidine photoproducts in solar UV-irradiated mammalian cells. Possible role of Dewar photoproducts in solar mutagenesis

Perdiz

Gróf

Mezzina

et al. 2000

Journal of Biological Chemistry

146

177

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“…At 5-min exposure, significantly no algal growth was observed. It is clear that UV light has a lethal effect on the cells' viability and created opportunities for optimal formation of morphological mutations due to its ability to induce highly efficient DNA damage with a survival curve of C-shape (Figures 1 and 2)/ This is in agreement with the reports of many researchers on the effect of UV light on algal microorganisms (Cadet et al, 1992;Danilchenko et al, 2002;Wu et al, 2005;Deng et al, 2011;IKehata and Ono, 2011). In exposing C. reinhardtii CC-124 to UV radiation with 5 W/m 2 for 1 to 5 min, out of 130 000 cells of C. reinhardtii strain, 14086 morphological surviving sub clones were formed.…”

Section: Resultssupporting

confidence: 81%

Generation and characterization of pigment mutants of Chlamydomonas reinhardtii CC-124

Zaydan¹,

Sadvakasova²,

Saleh³

et al. 2014

Afr. J. Biotechnol.

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The induced mutagenesis method for deriving pigment mutants of a green microalga, Chlamydomonas reinhardtii CC-124 and their pigment composition as well as ability to assess mutability of contaminated aquatic ecosystems were studied. In the present study, 14086 mutants (colonies) were obtained by exposure of the wild strain, C. reinhardtii CC-124, to 1, 2, 3, 5 min of ultraviolet (UV) irradiation. After screening, these mutants (colonies) revealed four pigmented mutants (124y-1, 124p-1, 124y-2 and 124p-2). Compared to the wild CC-124, these mutants are characterized by a decrease in chlorophyll a & b content and an increase in carotenoids. The lowest decrease in chlorophyll a was three to four folds, while the highest increase in carotenoids was two to four folds. The result of bio-test, using the resulting pigment mutant of C. reinhardtii 124y-1 showed that mutagenic activity was observed significantly in both Tekeli River and Pavlodar Oil Refinery in Kazakhstan; the waste water of the Pavlodar Oil Refinery had high-toxicity while the water of the Tekeli River had medium-toxicity.

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“…Depending on their stereochemistry, these BPDE-N 2 -guanine adducts are either accommodated in the minor groove (24) and cause DNA unwinding (17) or assume a base-displacement configuration with localized base pair disruption (25). For comparison, we also generated helix-destabilizing modifications by irradiating DNA with UV light at 254 nm, producing as major lesions cyclobutane pyrimidine dimers and pyrimidine(6-4) photoproducts in a ratio of about 3:1 (26).…”

Section: Nucleotide Excision Repair (Ner)mentioning

confidence: 99%

Recognition of DNA Adducts by Human Nucleotide Excision Repair

Gunz

Heß

Naegeli

1996

Journal of Biological Chemistry

187

147

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The mechanism by which mammalian nucleotide excision repair (NER) detects a wide range of base lesions is poorly understood. Here, we tested the ability of human NER to recognize bulky modifications that either destabilize the DNA double helix (acetylaminofluorene (AAF) and benzo[a]pyrene diol-epoxide (BPDE) adducts, UV radiation products) or induce opposite effects by stabilizing the double helix (8-methoxypsoralen (8-MOP), anthramycin, and CC-1065 adducts). We constructed plasmid DNA carrying a defined number of each of these adducts and determined their potential to sequester NER factors contained in a human cell-free extract. For that purpose, we measured the capacity of damaged plasmids to compete with excision repair of a site-directed NER substrate. This novel approach showed differences of more than 3 orders of magnitude in the efficiency by which helix-destabilizing and helixstabilizing adducts sequester NER factors. For example, AAF modifications were able to compete with the NER substrate ϳ1740 times more effectively than 8-MOP adducts. The sequestration potency decreased with the following order of adducts, AAF > UV BPDE > 8-MOP > anthramycin, CC-1065. A strong preference for helix-destabilizing lesions was confirmed by monitoring the formation of NER patches at site-specific adducts with either AAF or CC-1065. This comparison based on factor sequestration and repair synthesis indicates that human NER is primarily targeted to sites at which the secondary structure of DNA is destabilized. Thus, an early step of DNA damage recognition involves thermodynamic probing of the duplex. Nucleotide excision repair (NER)1 is an essential pathway for removing bulky base modifications from DNA. This repair mechanism involves endonucleolytic cleavage at two phosphodiester bonds, one 3Ј and the other 5Ј of the site of damage, followed by excision of DNA damage as the component of a single-stranded fragment (1-5). The excised oligonucleotide is replaced by DNA repair synthesis, and DNA continuity is reestablished by ligation. In mammalian cells, the major sites of incision are at the 5th phosphodiester bond 3Ј and the 24th phosphodiester bond 5Ј to the lesion (6).

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New trends in photobiology

Cited by 193 publications

References 106 publications

Distribution and repair of bipyrimidine photoproducts in solar UV-irradiated mammalian cells. Possible role of Dewar photoproducts in solar mutagenesis

Distribution and repair of bipyrimidine photoproducts in solar UV-irradiated mammalian cells. Possible role of Dewar photoproducts in solar mutagenesis

Generation and characterization of pigment mutants of Chlamydomonas reinhardtii CC-124

Recognition of DNA Adducts by Human Nucleotide Excision Repair

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