The Monte Carlo code PENELOPE has been used to simulate electron beams from a Siemens Mevatron KDS linac with nominal energies of 6, 12 and 18 MeV. Owing to its accuracy, which stems from that of the underlying physical interaction models, PENELOPE is suitable for simulating problems of interest to the medical physics community. It includes a geometry package that allows the definition of complex quadric geometries, such as those of irradiation instruments, in a straightforward manner. Dose distributions in water simulated with PENELOPE agree well with experimental measurements using a silicon detector and a monitoring ionization chamber. Insertion of a lead slab in the incident beam at the surface of the water phantom produces sharp variations in the dose distributions, which are correctly reproduced by the simulation code. Results from PENELOPE are also compared with those of equivalent simulations with the EGS4-based user codes BEAM and DOSXYZ. Angular and energy distributions of electrons and photons in the phase-space plane (at the downstream end of the applicator) obtained from both simulation codes are similar, although significant differences do appear in some cases. These differences, however, are shown to have a negligible effect on the calculated dose distributions. Various practical aspects of the simulations, such as the calculation of statistical uncertainties and the effect of the 'latent' variance in the phase-space file, are discussed in detail.

Since glutathione (GSH) protects against oxidative stress, we determined the regulation of cellular GSH by ionizing radiation in human hepatoblastoma cells, HepG2. The levels of GSH increased in irradiated HepG2 due to a greater Q Qglutamylcysteine synthetase (Q Q-GCS) activity, which was paralleled by Q Q-GCS heavy subunit chain (Q Q-GCS-HS) mRNA levels. Transcription of deletion constructs of the Q Q-GCS-HS promoter cloned in a reporter vector was associated with activator protein-1 (AP-1), consistent with the DNA binding of AP-1 in nuclear extracts of irradiated HepG2. Hence, the transcriptional regulation of Q Q-GCS by ionizing radiation emerges as an adaptive mechanism, which may be of significance to control the consequences of the oxidative stress induced by radiation.z 1998 Federation of European Biochemical Societies.