Abstract

Radiotherapy is effective on a large number of cancer types and is one of the most frequently administrated treatments for cancer patients. The anticancer efficacy of X-ray radiotherapy has been frequently correlated with reactive oxygen species (ROS) elevation, which is also a limiting factor for its toxicity on normal tissues. Here, we found that although 4-10 Gy X-rays could significantly reduce cell numbers in both MDA-MB-231 and MCF-7 breast cancer cells, the ROS level changes are less in MCF-7 cells than in MDA-MB-231 cells. Moreover, although both the ROS scavenger N-acetyl-L-cysteine (NAC) and 1 T static magnetic field (SMF) could reduce X-ray-induced ROS elevation, they did not prevent X-ray-induced cell number reduction or cell death increase, which is significantly different from cisplatin. These results demonstrate that although the anticancer efficacy of cisplatin on two breast cancer cell lines is dependent on ROS, the anticancer efficacy of X-ray is not. Moreover, by testing 19 different cell lines, we found that 1 T SMF could effectively reduce ROS levels in multiple cell lines by 10-20%, which encourages further studies to investigate whether SMF could be used as a potential “physical antioxidant” in the future.

Highlights

  • Radiotherapy has great advantages over chemotherapy for generating localized ionizing radiation on tumor tissues while fewer effects on normal tissues in the human body

  • The reactive oxygen species (ROS) levels in MCF-7 cells were increased by

  • The goal of the present study was to elucidate the role of ROS in response to X-ray exposure and cisplatin treatment and to determine the contribution of ROS in determining the anticancer efficacy of X-ray and chemodrug in breast cancer MDA-MB-231 and MCF-7 cells

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Summary

Introduction

Radiotherapy has great advantages over chemotherapy for generating localized ionizing radiation on tumor tissues while fewer effects on normal tissues in the human body. Different cell types and tissues respond to radiation differentially [3,4,5], the anticancer efficacy of X-ray radiotherapy has been frequently correlated with increased reactive oxygen species (ROS) and apoptosis [6,7,8,9,10,11,12]. ROS are highly reactive oxygen metabolites that include multiple types, such as superoxide radical, hydrogen peroxide, and hydroxyl radical. They are normal metabolic products during cell respiration, which are essential for some physiological cellular processes, but can be elevated in some pathological conditions or under external stresses

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