Bioradiation

1-Radiation Response on the Tissue Level
The appearance of radiation damage is related with two factors:

1-The biologic stress on the cell .
2-The conditions to which the cell is exposed pre and post irradiation

The time required for the tissue to respond to radiation damage can be predicted on the basis of the cell cycle kinetics of these critical cells, and there are three Biologic Factors moderating Cell injury by irradiation:

1- Cell cycle.
2- Intracellular repair.
3- Hypoxia.

2-Normal Tissue Response to Radiation
Normal tissue response to radiation classified on the time taken to exhibit clinical injury

1-Acute responding tissues: express injury during or within 2 - 3 weeks of the completion of radiotherapy e.g., skin, oral mucosa



2-Late responding tissues: express injury several months to years after irradiation e.g., kidney, lung, CNS








3-Biological Effects of Ion Irradiation

The biological effects depend on dose, ion type, LET, and the influence of the cell type .All effects will be discussed with respect to the particular physical characteristics of ion beams, i.e., track structure. Also environmental factors play vital role in Biological effects of ion irradiation. For Biological effect of Radiation the following Aspect should be take into account:
3-1 The Relative of Biological Effectiveness (RBE):

3-2 Systematic of RBE which includes:

3-2-1 Dose Dependence

3-2-2 Energy/LET Dependence
The increased RBE is not unique for all different kinds of charged particle radiation. Instead, it strongly depends on the particular physical characteristics of the ion beam .
3-2-3 Particle Dependence
3-2-4 Cell Type Dependence
These genetic differences lead to correspondingly different radio sensitivities after X-irradiation.

3-3- The Role of Increased Ionization Density

Increased ionization density was assumed to lead to more complex and thus less reparable damage.
3-3-1 Double Strand Break of DNA Induction and Rejoining
The increased ionization density to lead to a higher
Yield of severe damage, e.g., DSB (Double Strand Break)


3-3-2 Chromosome Aberrations
Investigation of chromosome aberrations also revealed the influence of radiation
quality on the rate of rejoining and repair of DSB., and leading also to the higher rate of exchange type aberrations between different chromosomes
3-4 Fractionated Irradiation
At least part of the damage can be repaired, leading to an overall decreased effect of fractionated compared to single dose exposure.
3- 5 Bystander Effects
The ‘bystander effect’ is used to describe situations where not only the primarily damaged cells respond to radiation, but also neighboring cells show a response without being directly damaged. The bystander effect could also
explain at least partially the hypersensitivity observed after irradiation with
charged particle beams at very low doses.












Figure 1:Bystander Effect


3-6 Tissue Effects
Cells in a tissue are usually connected by complex communication networks. In fact there are first indications that bystander effects cannot only be detected in in vitro systems, but also in in vivo-like systems such as, e.g., tissue explants Since bystander effects play a role at low doses and low influences, they might be in particular relevant for studies of mutation and transformation related to radiation protection .(Figure 2)

Figure 2: Mechanism of radiation effect on Tissue


4-Models of Biological Action of Radiation
Modeling plays an important role for the mechanistic understanding of radiation action as well as for practical applications in radiation protection and radiotherapy.

4-1 Dual Radiation Action
Based on the analysis of chromosome aberrations, the first models specifically based on lesion interaction. Estimates revealed that interaction should take place over distances of typically micrometers, so that the distribution of damage on a micrometer scale was thought to be of particular importance. Since the spatial distribution of damage cannot be investigated directly, the spatial distribution of energy deposition was taken as a measure reflecting the damage distribution. Among others, this is a theory of dual radiation action (TDRA).

4-2 Cluster Models
Clusters of damage should then result from clusters of energy deposition, and thus several models have been developed which are particularly based on detailed investigations of cluster properties of high-LET radiation with nanometer resolution.

4-3 Irregular Track Structure Models
Another class of models called ‘amorphous track structure’ models. The two key features of these models are:


A-They make use of the particular features of track structure in a certain simplified.

B- They are based on the assumption that no principle difference between the biological actions of low- and high-LET radiation exists, because in both cases the biological effect is due to the action of the secondary electrons. homogenous distribution of sensitivity throughout the nucleus is assumed as a first approximation.




















Figure 3: Direct and Indirect effect of Radiation.