Chelation of lysosomal iron protects against ionizing radiation.

Ionizing radiation causes DNA damage and consequent apoptosis, mainly due to the production of hydroxyl radicals (HO•) that follows radiolytic splitting of water. However, superoxide (O2•-) and H2O2 also form and induce oxidative stress with resulting LMP (lysosomal membrane permeabilization) arising from iron-catalysed oxidative events. The latter will contribute significantly to radiation-induced cell death and its degree largely depends on the quantities of lysosomal redox-active iron present as a consequence of autophagy and endocytosis of iron-rich compounds.

Different G2/M accumulation in M059J and M059K cells after exposure to DNA double-strand break-inducing agents.

Purpose: To investigate and compare the cell cycle progression in relation to cell death in the human glioma cell lines, M059J and M059K, after exposure to DNA double-strand break-inducing agents.

Methods And Materials: The M059J and M059K cells, deficient and proficient in the catalytic subunit of the DNA-dependent protein kinase, respectively, were exposed to 1 and 4 Gy of photons or accelerated nitrogen ions. In addition, M059J and M059K cells were treated with 10 and 40 mug/mL of bleomycin for 30 min, respectively.

Radiation-induced cell cycle response in lymphocytes is not related to clinical side-effects in breast cancer patients.

Background: We examined whether development of radiation-induced lung injury after irradiation for breast cancer correlates with lymphocyte radiosensitivity (LRS) in vitro.

Materials And Methods: Patients were selected from a cohort of 177 patients, who were treated with adjuvant postoperative radiotherapy (RT) for loco-regional breast cancer, and included 14 patients who had severe early lung injury measured as respiratory symptoms caused by RT and treated with corticosteroids (i.e.

X-ray-induced DNA double-strand breaks in mouse l1210 cells: a new computational method for analyzing neutral filter elution data.

The aim of this article is to present a method for studying the shape of the dose and repair responses for X-ray-induced double-strand breaks (DSBs) as measured by neutral filter elution (NFE). The approach is closely related to a method we developed for the use of specific molecular size markers and used for determination of the absolute number of randomly distributed radiation-induced DSBs by pulsed-field gel electrophoresis (PFGE). Mouse leukemia L1210 cells were X-irradiated with 0-50 Gy.