Abstract
Gold nanoparticles (GNPs), have been demonstrated as effective preclinical radiosensitising agents in a range of cell models and radiation sources. These studies have also highlighted difficulty in predicted cellular radiobiological responses mediated by GNPs, based on physical assumptions alone, and therefore suggest a significant underlying biological component of response. This study aimed to determine the role of mitochondrial function in GNP radiosensitisation. Using assays of DNA damage and mitochondrial function through levels of oxidation and loss of membrane potential, we demonstrate a potential role of mitochondria as a central biological mechanism of GNP mediated radiosensitisation.
Highlights
The application of radiobiological principles in clinical oncology aims to describe the relationship between absorbed dose and the resulting biological responses of tumour and normal tissues (Hall & Giaccia 2012)
Dose enhancement factor (DEF) can vary with delivered dose, and are quoted with reference to the dose delivered to cells in the absence of Gold nanoparticle (GNP)
Radiosensitising effects of 1.9 nm GNPs To assess the efficacy of 1.9 nm GNPs as radiosensitisers, clonogenic cell survival assays were performed in three cancer cell lines
Summary
The application of radiobiological principles in clinical oncology aims to describe the relationship between absorbed dose and the resulting biological responses of tumour and normal tissues (Hall & Giaccia 2012). Central to the development of novel clinic approaches is improvement in the differential responses between normal and tumour tissue at a fixed dose, termed the therapeutic ratio. Improvements in the therapeutic ratio of radiotherapy have been driven by developments in both radiation biology and radiation physics which have translated into significant advances in targeted dose delivery, radiological imaging and biological effectiveness. GNPs are relatively easy to synthesize in a range of sizes, can be readily functionalised, and have been shown to passively accumulate in tumours through the enhance permeability and retention effect (EPR) (Maeda et al 2000)
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