Some UV-bystander effects are mediated through induction of antioxidant defense in mammalian cells.

Bystander effect is the communication of signals from irradiated to unexposed neighboring cells which is often mediated through factors released from irradiated cells. We have attempted to investigate whether UV-bystander phenomenon can modulate the sensitivity of A375 cells and its mechanism. For this purpose, the conditioned medium from UVC-irradiated cells, which contained these released factors, was used to treat non-exposed cells. These cells were then subsequently treated with UVC or another genotoxicant H2O2. Cell viability was determined by Trypan blue-exclusion assay, DNA damage by flow cytometry analysis, ROS production by flow cytometry and microscopic analysis. Lipid peroxidation and antioxidant defense were assayed biochemically. Our findings revealed that exposure of non-irradiated cells to these factors induced increased in SOD and catalase activities which reverted to normal levels by 8 h. During this period, the released factors-treated cells were resistant to killing by UVC or H2O2 and induced DNA damage and lipid peroxidation were also lowered. This protection from cell killing was not present 8 h after exposure to these released factors. Our results suggested UV-bystander effect increased viability of cells through induction of antioxidant defense. This indicated UV-bystander phenomenon triggers protective response in cells.

Phenomenological explanation of cell inactivation cross section in terms of direct and indirect action

The aim of this study was to use survival curves data for the inactivation of V79 cells and CHO-K1 cells by protons, neutrons, C12 ions and He3 ions to study the role of direct and indirect action in cell inactivation. A large number of survival curves for the inactivation of V79 cells by protons, neutrons, and C12 ions and for CHO-K1 cells inactivated by He3 ions over a wide energy range were taken from published references. Experimental data points were extracted from the published survival curves using MATLAB [Version 7.0] and fitted to the linear quadratic equation. The fit parameters were used to calculate the inactivation cross section [segma] at the initial slope, the 2Gy dose and at 10% survival for each particle type separately. The results, in general, showed that the inactivation cross section decreases nearly exponentially when increasing the mean free path for primary ionisation [lamda], except in the case of protons, and to some extent neutrons, where the cross section takes a constant value at specific lamda values. The cross section increased with increasing linear energy transfer [LET] and also became independent of LET at specific LET values. The results indicate that the cell damage due to the double strand breaks of DNA caused by indirect action is much larger than that caused by the direct action

Accelerated proliferation correction factors in linear-quadratic and multiple-component models

Study in design to incorporate accelerated proliferation correction factors into linearquadratic and multiple-component models. Accelerated proliferation rate correction factor has been incorporated into the linearquadratic and the multiple component models by applying accelerated exponential cell growth to explain the tumor cell kinetics and estimates proper treatment results. Biological effectiveness and tumor control probability, in terms of BED [LQ model], BRD [MC model], TCP[LQ model] and TCP[MC model], were computed for three conventional and two accelerated hyperfractionated radiation therapy treatment schedules with using a range of accelerated proliferation rate constants to demonstrate the effect of the proliferation process. The results of the study show that the accelerated proliferation rate reduces the effectiveness of a treatment schedule delivered in a prolonged period of time. Care should be taken in the selection of a treatment protocol for a patient of head and neck cancer with an account of the cell kinetics of the tumor

Cellular inactivation induced by H2O2 and active oxygen species generated by environmental stresses in bacteria

Oxyygen free radicals are highly reactive species that damage several cellular macromolecules and organelles, including membrane lipid peroxidation and produce DNA lesions. We have discussed here; i) The mechanism of radiation-induced cellular damage in bacteria through the intermediation of active oxygen species; ii) the cellular inactivation and the role of bacterial SOS and OxyR systems in the repair of lesions induced by H2O2 under low iron condition; iii) the lethal interaction between H2O2 and o-phenanthroline in E. coli; iv) the biological response induced by near-UV radiation mediated by active oxygen species and finally v) the mutagenic potential of popular plant extracts like guaraná (Paullinia cupana), mate (Ilex paraguariensis) and saiao (Kalanchoe brasiliensis), whose effects are eventually mediated by active oxygen species.

Aspectos biológicos y médicos básicos sobre las radiaciones ionizantes / Basic medical and biological aspects of ionizing radiation

Las radiaciones tienen gran utilidad en medicina, Sin embargo, existen fuentes radiactivas (como las industriales) que pueden provocar exposiciones accidentales a radiaciones ionizantes que a su vez pueden repercutir en el organismo. En este trabajo se hace una revisión sobre aspectos básicos que los médicos de cualquier especialidad (especialmente aquellos que laboran en instituciones hospitalarias) deberían conocer y poder reconocer

Efectos biológicos de la radiación láser de baja potencia al nivel celular / Biological effects of low power laser radiation on cells

Se presenta un resumen bibliográfico de las principales inveastigaciones publicadas sobre los efectos biológicos primarios que proporciona la radiación láser de baja potencia. Se describen los efectos bioeléctrico, bioenergético, bioquímico y bioestimulante. Se exponen los posibles mecanismos de acción al nivel celular