[en] The LNT hypothesis is the basic principle of all radiation protection policy. This theory assumes that all radiation doses, even those close to zero, are harmful in linear proportion to dose and that all doses produce a proportionate number of harmful mutations, i.e., mis- or unrepaired DNA alterations. The LNT theory is used to generate collective dose calculations of the number of deaths produced by minute fractions of background radiation. Current molecular biology reveals an enormous amount of relentless metabolic oxidative free radical damage with mis/unrepaired alterations of DNA. The corresponding mis/unrepaired DNA alterations produced by background radiation are negligible. These DNA alterations are effectively disposed of by the DNA damage-control biosystem of antioxidant prevention, enzymatic repair, and mutation removal. High-dose radiation injures this biosystem with associated risk increments of mortality and cancer mortality. Low-dose radiation stimulates DNA damage-control with associated epidemiologic observations of risk decrements of mortality and cancer mortality, i.e., hormesis. How can this 40-year-old LNT paradigm continue to be the operative principle of radiation protection policy despite the contradictory scientific observations of both molecular biology and epidemiology and the lack of any supportive human data? The increase of public fear through repeated statements of deaths caused by 'deadly' radiation has engendered an enormous increase in expenditures now required to 'protect' the public from all applications of nuclear technology: medical, research, energy, disposal, and cleanup remediation. Government funds are allocated to appointed committees, the research they support, and to multiple environmental and regulatory agencies. The LNT theory and multibillion dollar radiation activities have now become a symbiotic self-sustaining powerful political and economic force. (author)

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[en] Since the fifties, the prime concern of radiation protection has been protecting DNA from damage. UNSCEAR initiated a focus on biosystem response to damage with its 1994 report, ''Adaptive Responses to Radiation of Cells and Organisms''. The DNA damage-control biosystem is physiologically operative on both metabolic and radiation induced damage, both effected predominantly by free radicals. These adaptive responses are suppressed by high-dose and stimulated by low dose radiation. Increased biosystem efficiently reduces the number of mutations that accumulate during a lifetime and decrease DNA damage-control with resultant aging and malignancy. Several statistically significant epidemiologic studies have shown risk decrements of cancer mortality and mortality from all causes in populations exposed to low-dose radiation. Further biologic and epidemiologic research is needed to establish a valid threshold below which risk decrements occur. (author)

[en] Awareness of current nuclear molecular biology is essential for world health and conservation of resources. A brief overview of current radiobiology and statistically significant supportive studies of human epidemiology and low-dose immunotherapy of cancer are presented. The genes in every cell continuously undergo an immense amount of metabolic damage by reactive oxygen species (ROS) which is prevented, repaired and removed by a complex antimutagenic system. The UNSCEAR 1994 Report and recent studies provide extensive documentation of low-dose simulation of many cellular functions, including antioxidant prevention, enzymatic repair and apoptotic and immunologic removal of DNA damage. Our model of the homeostatic system that controls the enormous burden of relentless metabolic DNA damage, consistent with current published data, provides quantitative comparison of metabolic mutations and background radiation mutations. The quantitative damage produced by background radiation ROS is comparatively negligible and is controlled by the same antimutagenic system; a homeostatic system that is stimulated by a ten, or even a hundredfold increase in background radiation. This enhanced prevention of gene mutations by spatial and temporal differences of ionizing radiation ROS is associated with decreased mortality and decreased cancer mortality observed in populations exposed to low-dose radiation. The accumulation of mutations with aging gradually impairs DNA damage-control. This in turn increases the rate of accumulation that is associated with increased risk of cancer with the 3rd to the 5th power of age. Death from cancer at an early age is usually the result of severe genetic impairment of DNA damage-control. Similarly, high-dose, high dose rate radiation also increases the risk of cancer by exceeding the homeostatic capacity of the antimutagenic system. All epidemiologic surveys of populations with high background radiation in the United States, Brazil, China, India, and Iran have observed no increased or even lower mortality and cancer than in control populations with low background radiation. During the past decade decreased mortality and decreased cancer in human populations exposed to low-dose radiation have been observed in large populations with high statistical power and careful consideration of controls: US-Japan Atomic Radiation Effect Research Foundation (RERF), East Urals Population Study, U.S. Nuclear Shipyard Worker Study, University of Pittsburgh Residential Radon Study, and the Canadian Breast Cancer Fluoroscopy Study. These epidemiologic observations of decreased cancer mortality and increased longevity of public, occupational, and medical cohort populations exposed to increased low-dose radiation are consistent with model prediction of radiation hormesis: a high background of 1.0 cGy/y decreased 0.1 cGy/y low background mutations from ∼ 1 to 0.8 mutations/cell/d with corresponding decreases of mortality and cancer mortality. Low-dose radiation immunotherapy prevents and removes cancer metastases in mice, rats, and humans. The health effects of radiation are not invariably negative in linear proportion to relatively small amounts of radiation-induced DNA damage. These health effects are determined by the biphasic dose response to low- and high-dose radiation of preventive, repair and removal cell functions of the homeostatic DNA damage-control system. (author)

[en] The cellular component of an acute ocular inflammation in rabbits was measured with autologous leukocytes exogenously labeled with ¹¹¹Indium tropolonate. Inflammation was induced by intravitreal bacterial lipopolysaccharide (LPS). After 16 hr blood was removed, leukocytes separated, labeled with ¹¹¹Indium tropolonate and reinjected. Three cell fractions were examined: a leukocyte rich fraction which had been prepared with Dextran; and polymorphonuclear and mononuclear leukocyte fractions which had been prepared using a discontinuous Percoll gradient. Two hours after labeled leukocytes were injected, measurements of ¹¹¹Indium were made in blood, plasma, the whole eye and in ocular compartments. From these data the numbers of each leukocyte population present were estimated and compared directly to histopathologic changes. Both polymorphonuclear and mononuclear leukocytes entered ocular tissues during the 2 hr period beginning 20 hr after LPS injection. Altered ocular vascular permeability was successfully measured with ¹²⁵Iodine-albumin in some of these same rabbits. Both the number and type of inflammatory cell entering ocular tissues during a set period of time of the inflammatory response could thus be measured. This technique provides an opportunity to define the relationship of leukocyte infiltration and altered ocular vascular permeability in ocular tissues during the inflammatory response

[en] Biological data obtained principally with Fe-59 citrate are used with physical data to calculate radiation absorbed doses for ionic or weak chelate forms of Fe-52, Fe-55, and Fe-59, administered by intravenous injection. Doses are calculated for normal subjects, primary hemochromatosis (also called idiopathic or hereditary hemochromatosis), pernicious anemia in relapse, iron-deficiency anemia, and polycythemia vera. The Fe-52 doses include the dose from the Mn-52m daughter generated after injection of Fe-52. Special attention has been given to the dose to the spleen, which has a relatively high concentration of RBCs and therefore of radioiron, and which varies significantly in size in both health and disease

[en] We present what we believe is the first reported case of a spontaneous aortoduodenal fistula, with massive rupture into the duodenum during the performance of a radionuclide study of gastrointestinal bleeding. Our experience suggests that nuclear scintigraphy with labeled red blood cells can help in the diagnosis of this disorder by demonstrating both the presence of an abdominal aortic aneurysm and bleeding in the gut

[en] Short communication

No abstract available