PubMed · 8305008
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P H Abelson. 1993-07-23. Toxic terror; phantom risks.. https://doi.org/10.1126/science.8305008
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Although well-established as carcinogens, the way in which chromium (VI) compounds exert their carcinogenic, mutagenic, and DNA-damaging potential remains obscure. It is clear that inside cells chromium(VI) is activated to its ultimate carcinogenic form by reducing agents including glutathione (GSH). The present study is intended to clarify if Fenton mechanisms are likely to be important in the formation of DNA lesions by chromium(VI) in combination with GSH. In buffer solutions which were treated to remove Fenton-active metal ions as well as in those not further purified, chromate and GSH induced similar numbers of single-strand breaks (SSB) in isolated PM2 DNA. Molecular oxygen was found to be essential for the formation of SSB, but chromium(V) species arising from chromate/GSH, unless activated by oxygen, appeared to be unreactive toward DNA. Upon addition of Mn(II) to solutions of chromium(VI) and GSH a diminution of Mn(II) ESR signals was observed, good evidence for the presence of chromium(IV) species. Using gas chromatography/mass spectrometry in selective ion-monitoring mode and high-performance liquid chromatography with electrochemical detection, we were able to show that Cr(VI)/GSH failed to induce base modifications typical of hydroxyl radical attack on DNA. Experimental conditions which readily induced SSB gave rise to the formation of chromium-DNA adducts, clearly demonstrating that the generation of these two DNA lesions is not mutually exclusive. We conclude that models which ascribe the induction of chromium-DNA adducts to chromium(V) and the generation of oxidative DNA damage including SSB to hydrogen peroxide are oversimplistic. It is not necessary to invoke a mechanism requiring the presence of added hydrogen peroxide to account for the ability of Cr(VI)/GSH to cause SSB. Our findings suggest that the combination of GSH, molecular oxygen, and chromium(VI) can damage DNA via non-Fenton pathways.
The minor role of the cancer research community in efforts to control human cancer by testing chemicals in rote bioassays and empirical "carcinogen" labelling is discussed. Although the causation of certain cancers by chemical carcinogens was a prominent segment of cancer research for many years this is no longer the case. The field has become the province of governmental regulators and little evidence suggests that an impact on the incidence of human cancer has resulted. In spite of a promising beginning major changes seem necessary; hopefully the cancer research community will become interested again and will reintroduce scientific disciplines into this area.
This paper reviews the recent progress of passive measurement methods of gamma radiation and radon. Relatively cheap and reliable dosimeters are now available. Results from national and world-wide surveys of natural radiation in bedrock and soils and indoor radon concentrations exist. These can be used to more precisely indicate areas with enhanced exposure to gamma radiation, indoor radon levels and radium and radon in household water. Besides direct measurements of the radiation intensity, additional information (e.g., history of residence, house ventilation habits) is required to reconstruct historical exposure levels for epidemiological investigations. The availability and correctness of this information may influence the validity of exposure estimates.