Inhalation Carcinogenesis of High-Fired 238 PuO 2 in Rats

Sanders, C.L.; Dagle, G.E.; Cannon, W.C.; Powers, G.J.; Meier, D. M.

doi:10.2307/3574622

Cited by 19 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Using the lowest two dose groups reported by Muggenburg et al (1996) for 238 PuO 2 alpha-particle-induced lung cancer in beagle dogs, a slope parameter of 1.7 × 10 -4 ± 1.0 × 10 -5 mGy -1 was obtained and is consistent with the result obtained for rats and humans. Using the lowest four dose groups reported by Sanders et al (1977) for 238 PuO 2 alpha-particleinduced lung cancer in Wistar rats, a slope parameter of 1.5 × 10 -4 ± 1.3 × 10 -4 mGy -1 was obtained and is consistent with other estimates summarized in Table 2. For the indicated exposure groups used by Sanders et al (1976), group average alpha radiation doses to the lung range from 50 to 1530 mGy.…”

Section: Resultssupporting

confidence: 69%

“…Alpha radiation administered alone is a potent inducer of lung cancer. Small doses (close to natural background radiation levels) can cause a significant increased incidence (Sanders et al 1976(Sanders et al , 1977Lundgren et al 1991;Sanders 2007). However, for combined exposure to low-dose alpha and low-dose gamma rays, the gamma-ray ANP could possibly prevent cancer induction by alpha radiation.…”

Section: Computational and Statistical Approachesmentioning

confidence: 99%

See 1 more Smart Citation

Low-Dose-Radiation Stimulated Natural Chemical and Biological Protection against Lung Cancer

Scott

2008

Dose-Response

View full text Add to dashboard Cite

Research is being conducted world-wide related to chemoprevention of future lung cancer among smokers. The fact that low doses and dose rates of some sparsely ionizing forms of radiation (e.g., x rays, gamma rays, and beta radiation) stimulate transient natural chemical and biological protection against cancer in high-risk individuals is little known. The cancer preventative properties relate to radiation adaptive response (radiation hormesis) and involve stimulated protective biological signaling (a mild stress response). The biological processes associated with the protective signaling are now better understood and include: increased availability of efficient DNA double-strand break repair (p53-related and in competition with normal apoptosis), stimulated auxiliary apoptosis of aberrant cells (presumed p53-independent), and stimulated protective immune functions. This system of low-dose radiation activated natural protection (ANP) requires an individual-specific threshold level of mild stress and when invoked can efficiently prevent the occurrence of cancers as well as other genomic-instability-associated diseases. In this paper, low, essentially harmless doses of gamma rays spread over an extended period are shown via use of a biological-based, hormetic relative risk (HRR) model to be highly efficient in preventing lung cancer induction by alpha radiation from inhaled plutonium.

show abstract

Section: Resultssupporting

confidence: 69%

Section: Computational and Statistical Approachesmentioning

confidence: 99%

Low-Dose-Radiation Stimulated Natural Chemical and Biological Protection against Lung Cancer

Scott

2008

Dose-Response

View full text Add to dashboard Cite

show abstract

“…From these assumptions the mean a-ray doses to lung for the 194µg enriched uranium group would have been 1500 to 1750 rad . Lung doses as great as this would probably be sufficient without the fission fragments to cause some of the squamous cell tumours observed in this group (table 1), since such tumours were also seen in the lungs of rats exposed to less than 2000 rad of a-rays alone from inhaled particles of plutonium oxide (Sanders et al 1976(Sanders et al , 1977 . From Sanders' experiments, however, it looks unlikely that a-ray doses of less than 2000 rad to the lung would be sufficient to make the incidence of squamous cell carcinoma so much greater than that for adenocarcinoma, as occurred in the 194 pg enriched uranium group .…”

Section: 2 2 Squamous Cell Carcinoma Of the Lungmentioning

confidence: 91%

“…Sanders et al . (1976Sanders et al . ( , 1977, using similar a-ray exposures of the lung from 239 PuO 2 or 238 PuO 2 in inhalation experiments, reported incidences of about 10 per cent for pulmonary adenocarcinoma which is broadly in agreement with the incidence in our rats receiving the uranium oxide only .…”

Section: 2 2 Squamous Cell Carcinoma Of the Lungmentioning

confidence: 96%

The Carcinogenic Effect of Localized Fission Fragment Irradiation of Rat Lung

Batchelor

Buckley

Gore

et al. 1980

International Journal of Radiation Biology and Related Studies

View full text Add to dashboard Cite

In a preliminary investigation of 'hot particle' carcinogenesis uranium oxide particles were introduced into the lungs of rats either by intubation of a liquid suspension of the particles or by inhalation of an aerosol. Subsequently the animals were briefly exposed to slow neutrons in a nuclear reactor, resulting in localized irradiation of the lung by fission fragments emitted from 235U atoms in the oxide particles. The uranium used in the intubation experiments was either enriched or depleted in 235U. Squamous cell carcinomas developed at the site of deposition of the enriched uranium oxide in many cases but no lung tumours occurred in the rats with the depleted uranium oxide, in which the lung tissue was exposed to very few fission fragments. Only enriched uranium oxide was used in the inhalation experiments. Pulmonary squamous cell carcinomas occurred after the fission fragment irradiation but were fewer than in the intubation experiments. Adenocarcinomas of the lung were seen in rats exposed to uranium oxide without subsequent irradiation by neutrons in the reactor and in rats irradiated with neutrons but not previously exposed to uranium oxide. It is concluded that (i) fission fragments were possibly implicated in the genesis of the squamous cell carcinomas, which only developed in those animals exposed to enriched uranium oxide and neutrons and (ii) the adenocarcinomas in the rats inhaling enriched uranium oxide only were likely to have been caused by protracted irradiation of the lung with alpha-rays emitted from the enriched uranium.

show abstract

Experimental Radiation Carcinogenesis

Silini

1986

Radiation Carcinogenesis and DNA Alterations

View full text Add to dashboard Cite

Inhalation Carcinogenesis of High-Fired 238 PuO 2 in Rats

Cited by 19 publications

References 0 publications

Low-Dose-Radiation Stimulated Natural Chemical and Biological Protection against Lung Cancer

Low-Dose-Radiation Stimulated Natural Chemical and Biological Protection against Lung Cancer

The Carcinogenic Effect of Localized Fission Fragment Irradiation of Rat Lung

Experimental Radiation Carcinogenesis

Contact Info

Product

Resources

About