Baradaran Samaneh, Maleknasr Niaz, Setayeshi Saeed, Akbari Mohammad Esmaeil
Dept. of Medical Radiation Engineering, Amirkabir University of Technology, Tehran, Iran ; National Radaition Protection Department, Iranian Nuclear Regulatory Authority, Tehran, Iran.
Faculty of Engineering, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Iran J Cancer Prev. 2014 Winter;7(1):40-7.
Alpha particle irradiation from radon progeny is one of the major natural sources of effective dose in the public population. Oncogenic transformation is a biological effectiveness of radon progeny alpha particle hits. The biological effects which has caused by exposure to radon, were the main result of a complex series of physical, chemical, biological and physiological interactions. The cellular and molecular mechanisms for radon-induced carcinogenesis have not been clear yet.
Various biological models, including cultured cells and animals, have been found useful for studying the carcinogenesis effects of radon progeny alpha particles. In this paper, sugars cape cellular automata have been presented for computational study of complex biological effect of radon progeny alpha particles in lung bronchial airways. The model has included mechanism of DNA damage, which has been induced alpha particles hits, and then formation of transformation in the lung cells. Biomarkers were an objective measure or evaluation of normal or abnormal biological processes. In the model, the metabolism rate of infected cell has been induced alpha particles traversals, as a biomarker, has been followed to reach oncogenic transformation.
The model results have successfully validated in comparison with "in vitro oncogenic transformation data" for C3H 10T1/2 cells. This model has provided an opportunity to study the cellular and molecular changes, at the various stages in radiation carcinogenesis, involving human cells.
It has become well known that simulation could be used to investigate complex biomedical systems, in situations where traditional methodologies were difficult or too costly to employ.
氡子体的α粒子辐射是公众人群有效剂量的主要自然来源之一。致癌转化是氡子体α粒子撞击的生物学效应。接触氡所引起的生物学效应是一系列复杂的物理、化学、生物和生理相互作用的主要结果。氡致致癌作用的细胞和分子机制尚不清楚。
已发现包括培养细胞和动物在内的各种生物学模型可用于研究氡子体α粒子的致癌作用。本文提出了糖被细胞自动机，用于对肺支气管气道中氡子体α粒子的复杂生物学效应进行计算研究。该模型包括α粒子撞击诱导的DNA损伤机制，以及随后肺细胞中转化的形成。生物标志物是对正常或异常生物学过程的客观测量或评估。在该模型中，作为生物标志物，受感染细胞的代谢率因α粒子穿过而被诱导，随后达到致癌转化。
与C3H 10T1/2细胞的“体外致癌转化数据”相比，该模型结果已成功得到验证。该模型为研究辐射致癌过程中涉及人类细胞的各个阶段的细胞和分子变化提供了机会。
众所周知，在传统方法难以应用或成本过高的情况下，模拟可用于研究复杂的生物医学系统。
