Potentially lethal damage repair and its inhibitory effect of caffeine in two yolk sac tumor cell lines with different radiosensitivities

Cancer Lett. 1999 Dec 1;147(1-2):199-206. doi: 10.1016/s0304-3835(99)00308-0.

Abstract

Purpose: In order to investigate the role of potentially lethal damage repair (PLDR) in cellular radiosensitivity, PLDR and its inhibitory effect by caffeine was examined. In addition, cell cycle distribution was also examined.

Materials and methods: Two rat yolk sac tumor cell lines, NMT-1 and NMT-1R, with different radiosensitivities in vitro were used. The capacity for PLDR was examined using confluent-phase cells, and evaluated by calculating the recovery ratio. Inhibitory effect of caffeine on PLDR was examined with doses of 1, 5 and 10 mM.

Results: The capacity of PLDR in two cell lines reflected radiosensitivity. The recovery ratio after irradiation of 5 Gy was 2.8 in the radiosensitive NMT-1 and 5.2 in the radioresistant NMT-1R, and recovery reached its peak level at 6 h in both cell lines. The degree of inhibition of PLDR was weaker in NMT-1R than that in NMT-1 at the same dose level, and was correlated with reduction of G2-arrested cells by caffeine.

Conclusions: The results of this study suggest that the capacity of PLDR may be one of the determinant factors for radiosensitivity in the two cell lines used, and the inhibitory effect of caffeine on PLDR was in part attributable to the modification of the cell cycle progression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caffeine / pharmacology*
  • Cell Cycle / drug effects
  • Cell Cycle / radiation effects
  • DNA Repair / drug effects*
  • DNA Repair / radiation effects*
  • Dose-Response Relationship, Drug
  • Dose-Response Relationship, Radiation
  • Endodermal Sinus Tumor / metabolism*
  • Endodermal Sinus Tumor / pathology
  • Endodermal Sinus Tumor / radiotherapy
  • Radiation Tolerance / drug effects*
  • Rats
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Caffeine