Cannabinoid receptors and their ligands: Role in cancer proliferation

Abstract

The primary mechanism of the biological effect of ionizing radiation has been known for more than 50 years: it is damage to DNA. In pharmaco-toxicological terms DNA is the “receptor” for radiation effects. Despite this knowledge, the current model for predicting or explaining health effects in populations exposed to internal exposures relies only upon quantifying radiation as average energy transfer to large masses of human tissue with no consideration whatever of the ionization density at the DNA relative to cytoplasm or non-DNA regions. This approach is equivalent to describing all chemical toxicological effects in terms of Mass and is clearly absurd. The concept of Radiochemical Genotoxicity is presented whereby biochemical affinity of internal radionuclides for DNA confers an excess genetic hazard which can be assessed. The most directly measurable effects of radiation exposure are heritable effects detectable around birth. Data enabling the development of a risk coefficient for internal exposures to Uranium fissionproducts is already available. By directly employing a meta-analysis of more than 19 epidemiological studies of post-Chernobyl birth outcomes in 10 different countries affected by contamination from Chernobyl a generalized risk coefficient for heritable damage is obtained. It is shown that the dose response is biphasic due to death of the foetus before term. The resulting coefficient is 20 per mSv internal exposure. Application of the new factor to the radionuclide exposures occurring during the period of atmospheric test contamination predicts the increases in infant mortality reported in the literature. The philosophical and ethical aspects are briefly discussed together with an account of the legal position in Europe.