High resolution proton nuclear magnetic resonance (1H NMR) spectroscopy of surviving C6 glioma cells after X-ray irradiation.

Purpose: To study biochemical response of living model of glioma to X-rays irradiation using high resolution proton nuclear magnetic resonance (1H NMR) spectroscopy.

Material And Methods: Rat glioma C6 cells were irradiated with 3.8 Gy (D0, the 37% clonogenic survival dose) of X-rays from a teletherapy unit at the dose rate 8.

Ionizing radiation-induced bystander effects, potential targets for modulation of radiotherapy.

Cells exposed to ionizing radiation show DNA damage, apoptosis, chromosomal aberrations or increased mutation frequency and for a long time it was generally accepted that these effects resulted from ionization of cell structures and the action of reactive oxygen species formed by water radiolysis. In the last few years, however, it has appeared that cells exposed to ionizing radiation and other genotoxic agents can release signals that induce very similar effects in non-targeted neighboring cells, phenomena known as bystander effects. These signals are transmitted to the neighboring non-hit cells by intercellular gap-junction communication or are released outside the cell, in the case of cultured cells into the medium.

[Radiation-induced bystander effect: the important part of ionizing radiation response. Potential clinical implications].

It has long been a central radiobiological dogma that the damaging effects of ionizing radiation, such as cell death, cytogenetic changes, apoptosis, mutagenesis, and carcinogenesis, are the results of the direct ionization of cell structures, particularly DNA, or indirect damage via water radiolysis products. However, several years ago attention turned to a third mechanism of radiation, termed the "bystander effect" or "radiation-induced bystander effect" (RIBE). This is induced by agents and signals emitted by directly irradiated cells and manifests as a lowering of survival, cytogenetic damage, apoptosis enhancement, and biochemical changes in neighboring non-irradiated cells.

[Oxidative stress in prostate hypertrophy and carcinogenesis].

Aging, significant impairment of the oxidation/reduction balance, infection, and inflammation are recognized risk factors of benign hyperplasia and prostate cancer. Chronic symptomatic and asymptomatic prostate inflammatory processes generate significantly elevated levels of reactive oxygen and nitrogen species, and halogenated compounds. Prostate cancer patients showed significantly higher lipid peroxidation and lower antioxidant levels in peripheral blood than healthy controls, whereas patients with prostate hyperplasia did not show such symptoms.