Radiation-induced heart disease in rats

Lauk, S.; Kiszel, Z.; Buschmann, Johannes; Trott, Klaus-Rüdiger

doi:10.1016/0360-3016(85)90314-1

Cited by 135 publications

(79 citation statements)

References 7 publications

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“…Exposure of mice to total physical doses of 0.2 Gy of 20 Ne, 1.6 Gy 40 Ar, and 3.2 Gy of 12 C resulted in structural injury to the coronary vessels 15 months after irradiation manifest as smooth muscle cell degeneration, fibrosis, and extracellular deposition (101). A single physical dose of 0.1 or 0.2 Gy of 56 Fe ions to the orbital region of the mouse results in degenerative changes in the coronary arteries 15 months after irradiation (100). These findings suggest that exposure to ions of iron at fluence rates relevant to those that would be encountered in space exploration results in late cardiovascular injury.…”

Section: Space Explorationmentioning

confidence: 99%

“…Radiation either directly to the thorax or specifically to the heart (18,37,55,56,103,104) will result in the development of injury after doses of 15 Gy and higher. A single exposure to 15-60 Gy exerts an adverse long-term effect on cardiovascular function in the rat, resulting in morphological degeneration (53), mechanical dysfunction (98), damage to the endothelium (9), and increased mortality (56). It has been suggested that radiation-induced cardiac injury is mediated by micro-vascular injury caused by inflammation and oxidative stress (6,75,81), but further studies are needed.…”

Section: Radiation As the Cause Of Late Cardiovascular Disease In Animentioning

confidence: 99%

“…Female mice have been reported to be more sensitive than male mice to the effects of 56 Fe ion irradiation (2-3 Gy) to the brain or hippocampal function (95). Female monkeys are more sensitive to the mortality effects of proton irradiation than males, with a dose effect occurring in the 0.25-1.13 Gy range, compared with a dose effect in the range of 3.6-4.0 Gy in males (105).…”

Section: Individual Radiation Sensitivity: Genetic and Gender Effectsmentioning

confidence: 99%

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Radiation as a Risk Factor for Cardiovascular Disease

Baker

Moulder

Hopewell

2011

Antioxidants & Redox Signaling

107

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Humans are continually exposed to ionizing radiation from terrestrial sources. The two major contributors to radiation exposure of the U.S. population are ubiquitous background radiation and medical exposure of patients. From the early 1980s to 2006, the average dose per individual in the United States for all sources of radiation increased by a factor of 1.7-6.2 mSv, with this increase due to the growth of medical imaging procedures. Radiation can place individuals at an increased risk of developing cardiovascular disease. Excess risk of cardiovascular disease occurs a long time after exposure to lower doses of radiation as demonstrated in Japanese atomic bomb survivors. This review examines sources of radiation (atomic bombs, radiation accidents, radiological terrorism, cancer treatment, space exploration, radiosurgery for cardiac arrhythmia, and computed tomography) and the risk for developing cardiovascular disease. The evidence presented suggests an association between cardiovascular disease and exposure to low-to-moderate levels of radiation, as well as the well-known association at high doses. Studies are needed to define the extent that diagnostic and therapeutic radiation results in increased risk factors for cardiovascular disease, to understand the mechanisms involved, and to develop strategies to mitigate or treat radiation-induced cardiovascular disease. Antioxid. Redox Signal. 15, 1945Signal. 15, -1956

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Section: Space Explorationmentioning

confidence: 99%

Section: Radiation As the Cause Of Late Cardiovascular Disease In Animentioning

confidence: 99%

Section: Individual Radiation Sensitivity: Genetic and Gender Effectsmentioning

confidence: 99%

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Radiation as a Risk Factor for Cardiovascular Disease

Baker

Moulder

Hopewell

2011

Antioxidants & Redox Signaling

107

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“…Radiation-induced damage to the microvasculature has severe pathological implications for kidney, heart and other tissues [8][9][10] . The most significant type of radiation-induced heart disease (RIHD) appears to be myocardial damage, which may result from loss of alkaline phosphatase activity of capillary endothelial cells 6−10 weeks after radiotherapy [9,11] . After a single dose of 20 Gy, myocardial degeneration becomes apparent in rats at approximately 6 months post-irradiation and is preceded by a marked reduction in capillary density [12] .…”

Section: Introductionmentioning

confidence: 99%

Hepatocyte growth factor protects endothelial cells against gamma ray irradiation-induced damage

Duan²,

Li³

et al. 2009

Acta Pharmacol Sin

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Aim: To investigate the effect of HGF on proliferation, apoptosis and migratory ability of human vascular endothelial cells against gamma ray irradiation. Methods: ECV304 cells derived from adult human umbilical vein endothelial cells (HUVEC) were irradiated with a single gamma ray dose of 20 Gy. Immunocytochemistry and Western blot analysis were used to detect c-Met protein expression and HGF/c-Met signal pathway. In the HGF-treated groups, ECV304 cells were incubated with HGF (20 or 40 ng/mL) 3 h prior to irradiation. At 48 h postirradiation, the proliferation of ECV304 cells was measured by MTT assay, the apoptosis was assessed by flow cytometry, and the migratory ability of ECV304 cells was measured by transwell chamber assay. Results: c-Met protein is expressed in ECV304 cells and can be activated by HGF. Gamma ray irradiation inhibits proliferation and migration of ECV304 cells in a dose-dependent manner. HGF significantly promoted the proliferation of ECV304 cells, and flow cytometry revealed that HGF can inhibit apoptosis of ECV304 cells. Transwell chamber assay also showed that HGF increases migration activity of endothelial cells. Conclusion: HGF may afford protection to vascular endothelial cells against gamma ray irradiation-induced damage.

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“…20-40 Gy) than a lower (<20 Gy) heart dose [14]. High-dose irradiation caused life-threatening radiation pericarditis, and the animals had to be sacrificed; no long-term follow-up results could be collected.…”

Section: The Pathomechanisms Of Radiation-induced Heart Disease (Rihd)mentioning

confidence: 99%

Experimental study of radiogenic heart damage using in vitro and in vivo animal models

Kiscsatári¹

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Radiation-induced heart disease in rats

Cited by 135 publications

References 7 publications

Radiation as a Risk Factor for Cardiovascular Disease

Radiation as a Risk Factor for Cardiovascular Disease

Hepatocyte growth factor protects endothelial cells against gamma ray irradiation-induced damage

Experimental study of radiogenic heart damage using in vitro and in vivo animal models

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