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Titolo:
A biomathematical modeling approach to explain the phenomenon of radiationhormesis
Autore:
Schollnberger, H; Menache, MG; Hanson, TE;
Indirizzi:
Salzburg Univ, Inst Phys & Biophys, A-5020 Salzburg, Austria Salzburg Univ Salzburg Austria A-5020 Biophys, A-5020 Salzburg, Austria Univ New Mexico, Sch Med, Dept Pediat, Albuquerque, NM 87131 USA Univ New Mexico Albuquerque NM USA 87131 ediat, Albuquerque, NM 87131 USA Univ New Mexico, Dept Math & Stat, Albuquerque, NM 87131 USA Univ New Mexico Albuquerque NM USA 87131 Stat, Albuquerque, NM 87131 USA
Titolo Testata:
HUMAN AND ECOLOGICAL RISK ASSESSMENT
fascicolo: 4, volume: 7, anno: 2001,
pagine: 867 - 890
SICI:
1080-7039(200108)7:4<867:ABMATE>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
STATE-VECTOR MODEL; DOSE IONIZING-RADIATION; ADAPTIVE RESPONSE; LUNG-CANCER; RESIDENTIAL RADON; DNA-DAMAGE; MECHANISMS; CARCINOGENESIS; IRRADIATION; LYMPHOCYTES;
Keywords:
radiation hormesis; Linear No-Threshold Theory; cellular defense mechanisms; endogenous DNA damage; U-shaped; radical scavenger;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Citazioni:
77
Recensione:
Indirizzi per estratti:
Indirizzo: Schollnberger, H Salzburg Univ, Inst Phys & Biophys, Hellbrunnerstr 34, A-5020 Salzburg, Austria Salzburg Univ Hellbrunnerstr 34 Salzburg Austria A-5020
Citazione:
H. Schollnberger et al., "A biomathematical modeling approach to explain the phenomenon of radiationhormesis", HUM ECOL R, 7(4), 2001, pp. 867-890

Abstract

This study presents an improved version of a published biomathematical model, the Random Coincidence Model-Radiation Adapted (RCM-RA). That model describes how cancer mortality increases as dose rate increases in the high-dose rate range, as well as how mortality decreases as dose rate increases inthe low-dose rate range. It was assumed that low-dose rates of ionizing radiation induce cellular defense mechanisms that also prevent or repair endogenous DNA damage caused by natural cell metabolism. The model presented describes the development of cancer by a phase of initiation that consists ofa series of DNA lesions in the critical regions of tumor-associated genes such as proto-oncogenes or tumor-suppressor genes. Initiated cells can divide and form a clone of initiated cells. This clonal growth is called promotion and leads to premalignant cells. Premalignant clones can sustain further genomic damage that may lead to a malignant cell and ultimately a malignant tumor. The model thereby shares structural features with Moolgavkar's two-stage clonal expansion model. It was tested on published, U-shaped data of radon exposure in U.S. homes. The model correctly reflects the ratio of endogenous DNA damage to radiation-induced damage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 19:59:40