Radiation induced bystander effect and DNA damage

Abstract

Bystander effects (BSEs) have been investigated for a long time but without much deliberation as to the cause in targeted cells and the subsequent effect in naïve cells. BSEs have traditionally been associated with radiation. Currently, this phenomenon is at a juncture where nuclear DNA damage is being debated as either essential or nonessential. If DNA damage is essential for the bystander signal (BSS) production then, this raises a number of questions about, radiotherapy and chemotherapy of cancer patients. This review presents a detailed analysis of the work done to investigate nuclear DNA damage versus exclusively cytoplasmic targeting with ionizing radiations and measurement of bystander end-points in naïve cells. The review also analyzes some of the research work done to investigate cell models that were developed specifically to study and track radiation-induced DNA damage to construct mutation spectra. Production of reactive oxygen species and reactive nitrogen species as possible candidates of the elusive BSS are also discussed besides the signal transduction pathways implicated in reception of a BSS by the naïve cell.

The different radiation response and radiation-induced bystander effects in colorectal carcinoma cells differing in p53 status

“…It has been even hypothesized that senescence-inducing mechanisms can be applicable in the future as cancer therapies by arresting the proliferation of cancer cells through senescence induction [9][10][11]. However, radiobiological data from the last several years show that radiation is able to induce response in adjacent cells and tissues not directly subjected to radiation, the phenomenon termed the radiation induced bystander effect [reviewed in [12][13][14][15][16][17][18][19]. This effect may be mediated by soluble factors released by irradiated cells into the extracellular environment and/or by the passage of mediating molecules through intercellular gap-junction communication channels.…”

Hepatitis C virus induces oxidative stress and DNA damage by regulating DNAPKCs, ATM, ATR and PARP mediated signaling and guards cell from cancerous condition by upregulating RB, P53 and downregulating VEGF

“…Current study involves establishment of HCV infected Huh-7 cell line and evaluating the mRNA expression of glutathione reductase (GSR), COX-2, retinoblastoma protein (RB), poly (ADPribose) polymerase (PARP) and VEGF. P53 has been shown to play a pivotal role in DNA damage repair pathways, including double strand breaks (DSBs), single strand breaks, base excision and mismatch repairs (Jalal et al, 2014). We hypothesized that HCV causes the oxidative stress, which in turn leads towards DNA damage (detected by DNA damage and repair genes ATM, ATR, DNAPKCs, PARP) and influences the expression of genes involved in carcinogenesis.…”

Palliative effects of lutein intervention in gamma-radiation-induced cellular damages in Swiss albino mice

“…The unexposed cells have also been shown to display the radiological changes when placed with the exposed cell media by the intercellular communication and also through the factors released by the exposed cells into the media. [11] The major studies have revealed that gamma radiation at sublethal doses, inflicted damages to the cell membrane,[12] increases the lipid peroxidation and reduces the total antioxidant capacity. [13] These effects are caused by the free radicals generated by radiolysis of water within the cell.…”