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Gene-Specific Repair of 6-4 Photoproducts in Trichothiodystrophy Cells
(Sheila Nathan),(Annmeke van Hoffen),(Leon H. F. Mullenders),(Lynne V. Mayne) 생화학분자생물학회 1999 BMB Reports Vol.32 No.6
TTDIBI cells are non-hypersensitive to UV irradiation and perform normal genome repair of pyrimidine dimers but fail to excise 6-4 photoproducts and, concomitantly, are unable to restore RNA synthesis levels following UV irradiation. This pointed to a defect in gene-specific repair and this study was undertaken to examine repair of 6-4 photoproducts at the gene-level. The results indicated a defect in gene-specific repair of 6-4 photoproducts in active genes, although strand-specificity of 6-4 photoproduct removal was essentially similar to that of normal cells. These findings indicate that the near normal UV resistance of TTDIBI cells may be due to the inability of these cells to remove DNA lesions preferentially, as well as to the cells opting out of the cell cycle to repair damage before resuming replication.
Gene-Specific Repair of 6-4 Photoproducts in Trichothiodystrophy Cells
Nathan,Sheila,Mullenders,Leon H. F.,Hoffen,Anneke van,Mayne,Lynne V. The Korea Science and Technology Center 1999 BMB Reports Vol.32 No.6
TTD1BI cells are non-hypersensitive to UV irradiation and perform normal genome repair of pyrimidine dimers but fail to excise 6-4 photoproducts and, concomitantly, are unable to restore RNA synthesis levels following UV irradiation. This pointed to a detect in gene-specific repair and this study was undertaken to examine repair of 6-4 photoproducts at the gene-level. The results indicated a defect in gene-specific repair of 6-4 photoproducts in active genes, although strand-specificity of 6-4 photoproduct removal was essentially similar to that of normal cells. These findings indicate that the near normal UV resistance of TTD1BI cells may be due to the inability of these cells to remove DNA lesions preferentially, as well as to the cells opting out of the cell cycle to repair damage before resuming replication.
Gene-Specific Repair of 6-4 Photoproducts in Trichothiodystrophy Cells
Nathan, Sheila,Van Hoffen, Anneke,Mullenders, Leon H.F.,Mayne, Lynne V. Korean Society for Biochemistry and Molecular Biol 1999 Journal of biochemistry and molecular biology Vol.32 No.6
TTD1BI cells are non-hypersensitive to UV irradiation and perform normal genome repair of pyrimidine dimers but fail to excise 6-4 photoproducts and, concomitantly, are unable to restore RNA synthesis levels following UV irradiation. This pointed to a detect in gene-specific repair and this study was undertaken to examine repair of 6-4 photoproducts at the gene-level. The results indicated a defect in gene-specific repair of 6-4 photoproducts in active genes, although strand-specificity of 6-4 photoproduct removal was essentially similar to that of normal cells. These findings indicate that the near normal UV resistance of TTD1BI cells may be due to the inability of these cells to remove DNA lesions preferentially, as well as to the cells opting out of the cell cycle to repair damage before resuming replication.
Antioxidant Effects of Garlic in Young and Aged Rat Brain In Vitro
Luigi Brunetti,Luigi Menghini,Giustino Orlando,Lucia Recinella,Sheila Leone,Francesco Epifano,Francesco Lazzarin,Annalisa Chiavaroli,Claudio Ferrante,Michele Vacca 한국식품영양과학회 2009 Journal of medicinal food Vol.12 No.5
Oxidative stress plays a key role in the pathogenesis of age-related neurodegeneration, and the nonenzymatic production of 8-iso-prostaglandin F2α (8-iso-PGF2α) may represent a reliable index of cellular oxidative damage. Garlic (Allium sativum) has been associated with peripheral antioxidant activities and therefore might prevent or reverse 8-iso-PGF2α production, but scant data are available on its possible neuroprotective effects. Therefore, we have studied the possible antioxidant effects of a garlic extract in rat brain synaptosomes obtained from young (3-month-old) and aged (14-month-old) male Wistar rats that were perfused, in vitro, with graded concentrations of a garlic extract (10–500μg/mL). Release in the effluent was evaluated, both in the basal state and after hydrogen peroxide-induced oxidative stress. In young rats, we observed a concentration-dependent inhibitory effect of the garlic extract on brain 8-iso-PGF2α production, both basally and after hydrogen peroxide-induced oxidative stimulus. In aged rats, 8-iso-PGF2α production was not affected by the garlic extract in the basal state, whereas, after hydrogen peroxide-induced oxidative stimulus, an antioxidant effect of the garlic extract appeared only at the higher concentration tested. In conclusion, garlic supplementation could be effective in preventing brain oxidative damage in young animals, whereas the aging brain seems to be resistant to the antioxidant effects of garlic, in vitro.