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Health Physics:
doi: 10.1097/HP.0b013e318222ad0a
Erratum

Session 3b: Propagation of Effects and Low Dose Impacts: Erratum

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In an article that appeared on page 289 in volume 100, number 3, there was an error in the text. The corrected text appears below:

This session was devoted to spontaneous and radiogenic perturbations of the physiological status of the system and its impact on cancer. Such a review can only touch on the wide range of topics discussed. Here it was discussed that most cellular and DNA damage appears to come from endogenous sources. The evolution of a variety of defenses designed to protect DNA and other critical molecules from attack by mutagens and toxins was widely discussed and is highlighted in the abstracts.

The role of oxidative stress was evaluated. Studies were reviewed that used repair deficient mice and concluded that some specific genes played a significant role in suppression of mutagenesis and tumorigenesis induced by oxidative stress. Data was discussed on up-regulation of antioxidants following exposures to low doses of ionizing radiation. Glutathione and γ-glutamyl synthetase as well as the superoxide dismutases and glutathione peroxidases were observed to be up-regulated following exposures to low doses/low fluences of different types of ionizing radiation. These can protect against both radiation and spontaneous damage.

The contribution of novel technologies in understanding the responses to low radiation doses was discussed and methods were evaluated on how to understand, use and analyze the data generated. The impact of low doses of radiation on mitochondrial functions (import, translation and activity of proteins in the mitochondria) was suggested as a potential mechanism for tissue specificity in radiation responses. The interactions of DNA repair and oxidative metabolism to protect DNA from oxidative damage was a major subject of discussion. The role of cell/cell and cell/matrix communication on interactions between co-cultured transformed and non-transformed cells was reviewed. These data suggest a potential mechanism of action for radiation-induced selective apoptosis of transformed cells through bystander modulated signaling events, involving TGF-β In these studies, non-transformed cells produced signals that resulted in selective apoptosis and killing of transformed cells. Thus, exposure to extremely low doses of radiation may selectively eliminate transformed cells and reduce low dose radiation risk.

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REFERENCE

Feinendegen LE, Brooks AL, Morgan WF. Session 3b: Propagation of Effects and Low Dose Impacts. Health Phys. 2011;100:289.

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