Chronic oxidative stress and radiation-induced late normal tissue injury: a review.
OBJECTIVE
It is proposed that the development and progression of radiation-induced late effects are driven, in part, by chronic oxidative stress. This mini-review presents data to support this hypothesis and provides the foundation for antioxidant-based interventional approaches directed at modulating late normal tissue injury.


CONCLUSIONS
Although a causal link between chronic oxidative stress and radiation-induced late normal tissue injury remains to be established, a growing body of evidence appears to support the hypothesis that chronic oxidative stress might serve to drive the progression of radiation-induced late effects. The similarity between chronic tissue injury, chronic inflammation and fibrosis observed in a variety of disease states, including radiation late effects, is provocative and offers the opportunity to apply antioxidant-based therapies to mitigate and/or treat late radiation-induced normal tissue injury.
Robbins
M E C
ME
Departments of Radiation Oncology and Neurosurgery, Brain Tumor Center of Excellence, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. mrobbins@wfubmc.edu
Zhao
W
W
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002493:Central Nervous System Diseases / Q000209:etiology / Q000378:metabolism; D002908:Chronic Disease; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000378:metabolism; D008171:Lung Diseases / Q000209:etiology / Q000378:metabolism; D009928:Organ Specificity; D018384:Oxidative Stress / Q000528:radiation effects*; D011832:Radiation Injuries / Q000378:metabolism* / Q000517:prevention & control*; D011839:Radiation, Ionizing; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012871:Skin Diseases / Q000209:etiology / Q000378:metabolism
D000975:Antioxidants; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species