The scid mutation in mice causes defects in the repair system for both double-strand DNA breaks and DNA cross-links

Mutat Res. 1993 Aug;288(2):277-80. doi: 10.1016/0027-5107(93)90095-w.

Abstract

The sensitivity of scid fibroblasts established from C.B17-scid/scid fetuses to the DNA-damaging agents bleomycin, neocarzinostatin, mechlorethamine, mitomycin C, methyl methanesulfonate, and ultraviolet light, all of which induce different types of DNA damage, was examined. Scid fibroblasts were 2.8-, 3.7-, and 3.0-fold more sensitive to bleomycin, neocarzinostatin, and mechlorethamine, respectively, than wild-type fibroblasts derived from C.B17-+/+ fetuses. These findings indicate that the scid mutation in mice causes defects in repairing both double-strand DNA breaks and DNA cross-links.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bleomycin / toxicity
  • Cell Line
  • Cell Survival / drug effects
  • DNA Damage*
  • DNA Repair*
  • Female
  • Male
  • Mechlorethamine / toxicity
  • Mice
  • Mice, SCID / genetics*
  • Mutation*
  • Pregnancy
  • Zinostatin / toxicity

Substances

  • Bleomycin
  • Mechlorethamine
  • Zinostatin