## 1 Introduction  
Over the last century, high-energy radiation, and in particular X-rays, has been utilized to treat cancer. The underlying concept is that rapidly proliferating cancer cells are more sensitive to X-rays than healthy cells [1]. X-ray irradiation of the cytoplasm causes radiolysis of water and gives rise to the formation of reactive oxygen species (ROS), including the super oxide radical (O\({}_{2}\)*), hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) and hydroxyl radical (HO\({}^{\bullet}\)). The most reactive one, HO\({}^{\bullet}\), provokes severe cellular damage, as it interacts with all biological molecules. This may give rise to lipid peroxidation, protein damage, deoxyribonucleic-acid strand breakages and membrane destruction which results in apoptotic and necrotic cell death. Despite substantial advances in the progress of novel cancer therapies such as the successful development of brachytherapy and intensity-modulated radiotherapy, nowadays, the greatest challenge is still to expose tumor cells to a lethal dose of X-rays while sparing normal cells [2]. An encouraging approach is the application of nanoparticulate radiosensitizers to tumor tissue which boosts the impact of X-rays on tumor cells [3; 4; 5; 6; 7; 8; 9]. Local dose enhancement in radiotherapy of cancer employs high-Z materials (e.g., gold, platinum, bismuth and gadolinium), as they exhibit a large photoelectric absorption coefficient [5]. Interaction between X-rays with moderate energies (10 to 500 keV) and high-Z gold atoms in nanoparticles generates secondary electrons, such as photoelectrons and Auger electrons [4; 8]. Since the range of these electrons is very short, they are highly effective in close proximity to gold nanoparticles inside the tumor cell. X-radiation-induced emission of these short-range electrons facilitates the deposition of highly localized energy into the cellular organelles, which inflicts irreversible damage to the targeted cells. On the other hand, due to their rapid decay within nanoscale volumes, these electrons cannot impair the surrounding healthy tissue. Therefore, gold nanoparticles (AuNPs) are auspicious candidates for application as radio-enhancers for X-rays in radiotherapy [6; 10; 11; 12]. The most effective reactive oxygen species (ROS), which are generated by X-ray irradiation of intracellular AuNPs, are the superoxide anion (O\({}_{2}^{\bullet}\)) and hydroxyl radical (HO\({}^{\bullet}\)). X-ray-triggered generation of photoelectrons and Auger electrons is understood to be responsible for the formation of O\({}_{2}^{\bullet}\) in the vicinity of gold nanoparticles, whereas the emitted characteristic X-radiation causes the formation of HO\({}^{\bullet}\) due to water radiolysis [13]. Among these ROS, the HO\({}^{\bullet}\) causes the greatest damage to tumor cells by oxidizing lipids, proteins and DNA [14]. In recent studies [15; 16], we could unambiguously prove that intracellular Fe\({}_{3}\)O\({}_{4}\) nanoparticles (SPIONs) enhanced the impact of X-radiation on tumor cells by significantly increasing the ROS production and, in particular, by raising the intracellular HO\({}^{\bullet}\) concentration. The radio-enhancing effect of the SPIONs originates from the catalytic activity of their surfaces. X-rays, even at 1 Gy, verifiably destroy the coating of intracellular SPIONs terminated with citrate or malate moieties. X-radiation-induced ablation of the surface layer of the SPIONs creates highly reactive surfaces containing Fe\({}^{3+}\) and Fe\({}^{2+}\) ions that catalyze the ROS formation via the Fenton mechanism and Haber-Weiss cycle. The ROS concentration was found to be increased by more than 300% [16]. Another encouraging approach for radio-enhancing nanomaterials is based on the fusion of plasmonic gold and superparamagnetic Fe\({}_{3}\)O\({}_{4}\) nanoparticles yielding Fe\({}_{3}\)O\({}_{4}\)-Au nanocomposites.