Literature DB >> 6700618

Abnormal sensitivity of some Cockayne's syndrome cell strains to UV- and gamma-rays. Association with a reduced ability to repair potentially lethal damage.

P J Deschavanne, N Chavaudra, B Fertil, E P Malaise.   

Abstract

Cockayne's syndrome (CS) is a rare autosomal recessive genetic disease characterized by mental and physical retardation, microcephaly, dwarfism, retinitis pigmentosa and a hypersensitivity to sunlight. Cells originating from patients also exhibit, in vitro, a hypersensitivity to UV radiation. Using a colony assay in vitro, we studied the sensitivity of 5 CS cell strains (GM739, BOR, CS697, CS698 and KA) and two normal ones (HF19 and GP) to UV- and gamma-irradiation. The 5 CS strains appear to be UV-hypersensitive but the sensitivity varies widely from one strain to another. Hypersensitivity to gamma-rays has been reported for 4 out of the 5 CS cell strains investigated. However, these CS cell strains are less sensitive to gamma-rays than are ataxia telangiectasia cells. The KA cell strain exhibits a normal response to gamma-irradiation. Repair of potentially lethal damage (PLD) after UV- and gamma-irradiation was investigated by using unfed plateau-cell cultures. Under these conditions, control cells show a great capacity to repair PLD (10- to 30-fold survival increase at 1% survival level). The two CS strains (GM739 and BOR), which are hypersensitive to both UV- and gamma-irradiation, exhibit no or only little PLD repair after treatment. In contrast, the normal response of KA cells to gamma-rays is associated with a normal PLD repair capability. This latter cell strain exhibits an intermediate sensitivity to UV and shows an intermediate PLD repair capacity. The response of CS cell strains after gamma-irradiation suggests a genetic heterogeneity. Three complementation groups are described in CS cells when dealing with UV radiosensitivity. However, variations in gamma-ray sensitivity are reported for cells within the same UV complementation group.

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Year:  1984        PMID: 6700618     DOI: 10.1016/0167-8817(84)90012-9

Source DB:  PubMed          Journal:  Mutat Res        ISSN: 0027-5107            Impact factor:   2.433


  5 in total

Review 1.  [Genetic predisposition and radiation sensitivity of tumors].

Authors:  W Budach
Journal:  Strahlenther Onkol       Date:  1997-09       Impact factor: 3.621

2.  Protein oxidative damage is associated with life expectancy of houseflies.

Authors:  R S Sohal; S Agarwal; A Dubey; W C Orr
Journal:  Proc Natl Acad Sci U S A       Date:  1993-08-01       Impact factor: 11.205

3.  Ultraviolet-induced mutations in Cockayne syndrome cells are primarily caused by cyclobutane dimer photoproducts while repair of other photoproducts is normal.

Authors:  C N Parris; K H Kraemer
Journal:  Proc Natl Acad Sci U S A       Date:  1993-08-01       Impact factor: 11.205

4.  The levels of repair of endonuclease III-sensitive sites, 6-4 photoproducts and cyclobutane pyrimidine dimers differ in a point mutant for RAD14, the Saccharomyces cerevisiae homologue of the human gene defective in XPA patients.

Authors:  S H Reed; S McCready; S Boiteux; R Waters
Journal:  Mol Gen Genet       Date:  1996-03-07

5.  Preferential repair of ionizing radiation-induced damage in the transcribed strand of an active human gene is defective in Cockayne syndrome.

Authors:  S A Leadon; P K Cooper
Journal:  Proc Natl Acad Sci U S A       Date:  1993-11-15       Impact factor: 11.205

  5 in total

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