Selenoprotein P inhibits radiation-induced late reactive oxygen species accumulation and normal cell injury.

ABSTRACT:

Purpose

Radiation is a common mode of cancer therapy whose outcome is often limited because of normal tissue toxicity. We have shown previously that the accumulation of radiation-induced late reactive oxygen species (ROS) precedes cell death, suggesting that metabolic oxidative stress could regulate cellular radiation response. The purpose of this study was to investigate whether selenoprotein P (SEPP1), a major supplier of selenium to tissues and an antioxidant, regulates late ROS accumulation and toxicity in irradiated normal human fibroblasts (NHFs).

Methods and materials

Flow cytometry analysis of cell viability, cell cycle phase distribution, and dihydroethidium oxidation, along with clonogenic assays, were used to measure oxidative stress and toxicity. Human antioxidan

SUBMITTER: Eckers JC 

PROVIDER: S-EPMC3787541 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature