Activation of immunological network by chronic low-dose-rate irradiation in wild-type mouse strains: analysis of immune cell populations and surface molecules. Ina Y, Sakai K. LDRC (Low Dose Radiation Research Center), CRIEPI (Central Research Institute of Electric Power Industry), Komae, Tokyo, Japan. hormesis@yasuhiro-ina-dmsc.jp PURPOSE: To analyse the effects of chronic whole body low-dose-rate irradiation on the immune system in various wild-type mouse strains in comparison with the effects from acute high-dose-rate irradiation. MATERIALS AND METHODS: Wild-type mouse strains (C57BL/6, BALB/c, C3H/He, DBA/1, DBA/2 and CBA) were observed after chronic low-dose-rate gamma irradiation at 1.2 mGy hour(-1) by intensive analysis of immune cell populations and their various surface molecules, together with antibody-producing activity both with and without immunization by sheep red blood cells (SRBC). The cell surface functional molecules [cluster of differentiation (CD) 3, CD4, CD8, CD19, CD45R/B220, intercellular adhesion molecule (ICAM)-1, Fas, natural killer (NK)-1.1, chemokine [C-X-C motif] receptor 4 (CXCR4) and chemokine [C-C motif] receptor 5 (CCR5)] and activation molecules [thymocyte-activating molecule (THAM), CD28, CD40, CD44H, CD70, B7-1, B7-2, OX-40 antigen, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), CD30 ligand and CD40 ligand] were studied in the bone marrow, thymus, spleen, lymph nodes and peripheral blood by flow cytometry. RESULTS: By chronic low-dose-rate irradiation alone, CD4+ T cells and CD8 molecule expression increased significantly by a maximum of 30%, while CD40+ B cells decreased significantly. Increases of CD4+ T cells, CD40+ B cells and anti-SRBC antibody-producing cells by immunization were significantly enhanced by continuous low-dose-rate irradiation at 1.2 mGy hour(-1). CD3- CD4+ T cells, representative of abnormal immune cells, were absent in the chronically low-dose-rate-irradiated mice, while a dose-dependent increase of these cells was found in acutely high-dose-rate-irradiated mice given the same total doses. CONCLUSION: Chronic low-dose-rate radiation activated the immune system of the whole body. Int J Radiat Biol. 2005 Oct;81(10):721-9. PMID: 16449079 [PubMed - indexed for MEDLINE] The myth and reality of reversal of aging by hormesis. Sonneborn JS. Department of Zoology & Physiology, University of Wyoming, Box 3663, 16th & Gibbon Street, Laramie, Wyoming 82071, USA. cancun@uwyo.edu Hormesis is an adaptive response to low doses of otherwise harmful agents by triggering a cascade of stress-specific resistance pathways. Evidence from protozoa, nematodes, flies, rodents, and primates indicate that stress-induced tolerance modulates survival and longevity. "Reality" is that hormesis can prolong the healthy life span. Genetic background provides the potential for longevity duration induced by stress. Senesence, or aging, is generally thought to be due to a different impact of selection for alleles positive for reproduction during early life but harmful in later life, a process called antagonistic pleiotropy (multiple phenotypic changes by a single gene). After reproduction, life span is "invisible" to selection. I propose the revision that mutations selected for survival until reproduction in early life may also extend later life (protagonistic pleiotropy). The protagonist candidate genes for extended life span are hormetic response genes, which activate the protective effect in both early and later life. My revision of the earlier evolutionary theory implies that natural selection of genes critical for early survival (life span until reproduction) can also be beneficial for extended longevity in old age, tipping the evolutionary balance in favor of a latent inducible life span extension unless excess stressor challenge exceeds the protection capacity. Mimetic triggers of the stress response promise the option of tricking the induction of metabolic pathways that confer resistance to environmental challenges, increased healthy life span, rejuvenation, and disease intervention without the danger of overwhelming damage by the stressor. Public policy should anticipate an increase in healthy life span. Ann N Y Acad Sci. 2005 Dec;1057:165-76. PMID: 16399893 [PubMed - indexed for MEDLINE] Remember we are NOT Doctors and have NO medical training. This site is like an Encylopedia - there are many pages, many links on many topics. Support our work with any size DONATION - see left side of any page - for how to donate. You can help raise awareness of CAM.