Abstract
Under acute perturbations from outer environment, a normal cell can trigger cellular self-defense mechanism in response to genome stress. To investigate the kinetics of cellular self-repair process at single cell level further, a model of DNA damage generating and repair is proposed under acute Ion Radiation (IR) by using mathematical framework of kinetic theory of active particles (KTAP). Firstly, we focus on illustrating the profile of Cellular Repair System (CRS) instituted by two sub-populations, each of which is made up of the active particles with different discrete states. Then, we implement the mathematical framework of cellular self-repair mechanism, and illustrate the dynamic processes of Double Strand Breaks (DSBs) and Repair Protein (RP) generating, DSB-protein complexes (DSBCs) synthesizing, and toxins accumulating. Finally, we roughly analyze the capability of cellular self-repair mechanism, cellular activity of transferring DNA damage, and genome stability, especially the different fates of a certain cell before and after the time thresholds of IR perturbations that a cell can tolerate maximally under different IR perturbation circumstances.
Highlights
A biological system consists of from a few copies to millions of different components with specific interactions
We simulate the dynamic kinetics of DNA damage generation, repair mRNA transcription, Repair Protein (RP) translation, DSB-protein complexes (DSBCs) synthesis and toxin accumulation
Kinetics of DNA damage generation In DNA damage generation process, we focus on illustrating the dynamic interactions between DNA and acute Ion Radiation (IR) perturbation from outer environment, the kinetics of Double Strand Breaks (DSBs) generation, DNA damage accumulation and DNA increasing without cellular selfrepair mechanisms, as well as repair gene decreasing against continuous IR perturbation
Summary
A biological system consists of from a few copies to millions of different components with specific interactions. In response to genome stress under acute perturbations from outer environment, a cell can start its internal self-defense mechanism triggered by complicated interactions among these ‘‘active particles’’ [2,3]. A normal cell can trigger its selfrepair mechanisms to fix DNA damage induced by external IR perturbation. As a main signal source of transferring genome stress, DSBC can relay DNA damage to downstream genes and their signal pathways. P53, a vital anti-cancer gene, can be activated by DSBCs transferring, and active P53 can prompt its downstream genes, and further control the cell cycle arrest and abnormal cell apoptosis in order to eliminate lethal genome damage or deregulated proliferation [6,7]
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