作者: Christine B Ambrosone , Chunqiao Tian , Jiyoung Ahn , Silke Kropp , Irmgard Helmbold
DOI: 10.1186/BCR1526
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摘要: Introduction The cytotoxic effects of radiation therapy are mediated primarily through increased formation hydroxyl radicals and reactive oxygen species, which can damage cells, proteins DNA; the glutathione S-transferases (GSTs) function to protect against oxidative stress. We hypothesized that polymorphisms encoding reduced or absent activity in GSTs might result greater risk for radiation-associated toxicity.