Low-Dose-Radiation Stimulated Natural Chemical and Biological Protection against Lung Cancer

Abstract

Research is being conducted world-wide related to chemoprevention of future lung cancer among smokers. The fact that low doses and dose rates of some sparsely ionizing forms of radiation (e.g., x rays, gamma rays, and beta radiation) stimulate transient natural chemical and biological protection against cancer in high-risk individuals is little known. The cancer preventative properties relate to radiation adaptive response (radiation hormesis) and involve stimulated protective biological signaling (a mild stress response). The biological processes associated with the protective signaling are now better understood and include: increased availability of efficient DNA double-strand break repair (p53-related and in competition with normal apoptosis), stimulated auxiliary apoptosis of aberrant cells (presumed p53-independent), and stimulated protective immune functions. This system of low-dose radiation activated natural protection (ANP) requires an individual-specific threshold level of mild stress and when invoked can efficiently prevent the occurrence of cancers as well as other genomic-instability-associated diseases. In this paper, low, essentially harmless doses of gamma rays spread over an extended period are shown via use of a biological-based, hormetic relative risk (HRR) model to be highly efficient in preventing lung cancer induction by alpha radiation from inhaled plutonium.

Radiation-Stimulated Epigenetic Reprogramming of Adaptive-Response Genes in the Lung: An Evolutionary Gift for Mounting Adaptive Protection against Lung Cancer

“…However, this system essentially ignores natural radiation protection and in doing so can lead to radiation-phobia associated casualties during radiological emergencies. Based on the material discussed herein and elsewhere (Ketchum 1987;Wolf et al 1988;Wolff 1989Wolff , 1992Wolff , 1996Luckey 1991;Mifune et al 1992;Hipp and Bauer 1997;Trosko 1998;Redpath et al 2001;Liu 2003;Sakai et al 2003;Scott 2004Scott , 2005Scott , 2007Scott , 2008Jaworowski 2006;Bauer 2007;Day et al 2007;Feinendegen 2005;Sakai 2006;Scott and Di Palma 2006;Feinendegen et al 2007;Liu 2007;Mitchel 2007;Portess et al 2007;;Strzelczyk et al 2007;Cohen 2008;Rithidech and Scott 2008;Sanders 2008;Sanders and Scott 2008;Scott et al 2008;Tubiana 2008), there is a need for a more scientifically valid, updated system of radiation protection that allows for radiation ANP. However, current radiation protection organizations continue to promote the LNT-based system in spite of its problems (Strzelczyk et al 2007).…”

Different radiosensitivity of CD4+CD25+regulatory T cells and effector T cells to low dose gamma irradiation in vitro

“…Low dose of gamma irradiation induces reactive oxygen species (ROS) and the activation of specific intracellular signaling pathways and transcription factors leading to proliferation and differentiation of target cells (Kasid et al 1996, Lander et al 1997, Finkel 1998). Therefore, gamma irradiation can modulate immune response via its variable effects on immune cell survival and differentiation (Shankar et al 1999, Rho et al 2004, Liu 2007, Shan et al 2007, Scott 2008). …”

Competitive principal of tumor control in radiological clinic

“…Since 1998, we have been proving indirect mechanism of diminishing the cancer activity by slightly increased natural or artificial background radiation and low dose total/subtotal radiation therapy. In oppose to idea of radiogenic stimulation of anti-cancer immunity [8,9], the mechanism proposed by us bases on the redistribution of circulating morphogenic cells from tumor to exposed normal tissues [10][11][12][13], and was statistically tested [14,15]. As a proliferative resource of bone marrow is limited and associated very closely with the life span and the level of lymphopenia [16,17], the HBI with cumulative dose 9 Gy was employed mostly as myelosuppressive one.…”