Modulation of oxidative phosphorylation (OXPHOS) by radiation- induced biophotons.

Radiation-induced biophotons are an electromagnetic form of bystander signalling. In human cells, biophoton signalling is capable of eliciting effects in non-irradiated bystander cells. However, the mechanisms by which the biophotons interact and act upon the bystander cells are not clearly understood.

Exosomes are released by bystander cells exposed to radiation-induced biophoton signals: Reconciling the mechanisms mediating the bystander effect.

Objective: The objective of our study was to explore a possible molecular mechanism by which ultraviolet (UV) biophotons could elicit bystander responses in reporter cells and resolve the problem of seemingly mutually exclusive mechanisms of a physical UV signal & a soluble factor-mediated bystander signal.

Methods: The human colon carcinoma cell line, HCT116 p53 +/+, was directly irradiated with 0.5 Gy tritium beta particles to induce ultraviolet biophoton emission.

An Observed Effect of p53 Status on the Bystander Response to Radiation-Induced Cellular Photon Emission.

In this study, we investigated the potential influence of p53 on ultraviolet (UV) signal generation and response of bystander cells to the UV signals generated by beta-irradiated cells. Five cell lines of various p53 status (HaCaT, mutated; SW48, wild-type; HT29, mutated; HCT116, wild-type; HCT116, null) were irradiated with beta particles from tritium. Signal generation (photon emission at 340 ± 5 nm) was quantified from irradiated cells using a photomultiplier tube.

Factors affecting ultraviolet-A photon emission from β-irradiated human keratinocyte cells.

The luminescence intensity of 340±5 nm photons emitted from HaCaT (human keratinocyte) cells was investigated using a single-photon-counting system during cellular exposure to (90)Y β-particles. Multiple factors were assessed to determine their influence upon the quantity and pattern of photon emission from β-irradiated cells. Exposure of 1 x 10(4) cells/5 mL to 703 μCi resulted in maximum UVA photoemission at 44.

An observed effect of ultraviolet radiation emitted from beta-irradiated HaCaT cells upon non-beta-irradiated bystander cells.

Previous research has shown that beta radiation can induce ultraviolet (UV) photon emission in human keratinocyte cells. Spectral analysis using a filter-based method in the ultraviolet range demonstrated that the strongest externally measureable photon emission was induced by beta radiation in the UVA range. In the current study, the potential biological implications of this UV photon emission from beta-irradiated cells were investigated.