Radiation hormesis: Autophagy and other cellular mechanisms

@article{Szumiel2012RadiationHA,
  title={Radiation hormesis: Autophagy and other cellular mechanisms},
  author={Irena Szumiel},
  journal={International Journal of Radiation Biology},
  year={2012},
  volume={88},
  pages={619 - 628}
}
  • I. Szumiel
  • Published 18 June 2012
  • Biology
  • International Journal of Radiation Biology
Abstract Purpose: To review the cellular mechanisms of hormetic effects induced by low dose and low dose rate ionising radiation in model systems, and to call attention to the possible role of autophagy in some hormetic effects. Results and conclusions: Very low radiation doses stimulate cell proliferation by changing the equilibrium between the phosphorylated and dephosphorylated forms of growth factor receptors. Radioadaptation is induced by various weak stress stimuli and depends on… 

Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

This review is focused on how energy, dose and quality of IR affect mitochondria-dependent epigenetic and functional control at the cellular and tissue level.

Molecular mechanisms of low dose ionizing radiation-induced hormesis, adaptive responses, radioresistance, bystander effects, and genomic instability

It is suggested that different manifestations of LDIR-induced cellular responses may have different signal transduction pathways and caution should be taken when designing therapeutic approaches using LDIR to induce beneficial effects in humans.

Possible role of NF-κB in hormesis during ageing

NF-κB plays a fundamental role in stress response, apoptosis and autophagy and appears to be a possible target for hormesis in ageing.

Radiation induces autophagic cell death via the p53/DRAM signaling pathway in breast cancer cells.

The p53/DRAM signaling pathway appears to contribute to radiation-induced autophagic cell death in MCF-7 breast cancer cells.

Hormesis in Aging and Neurodegeneration—A Prodigy Awaiting Dissection

Facilitated by a simple mathematical model, it is shown for the first time that ROS-mediated hormesis can be explained by the addition of different biomolecular reactions including oxidative damage, MAPK signaling and autophagy stimulation.

Low-dose ionizing radiation as a hormetin: experimental observations and therapeutic perspective for age-related disorders

It is argued here that assessment and clinical trials of LDIR treatments should be given priority bearing in mind the enormous economic, social and ethical implications of potentially-treatable, age-related disorders.

A concept of radiation hormesis: stimulation of antioxidant machinery in rats by low dose ionizing radiation.

Results clearly indicate that low dose X-rays radiation exposure stimulates endogenous antioxidant defense machinery and also causes an increase in whole blood lymphocytes and eosinophils responsible for providing key defenses.

Life History Trade-offs within the Context of Mitochondrial Hormesis.

It is proposed that there is limited support for the hypothesis that reproduction generates free radicals that cause oxidative stress and, in turn, oxidative stress damages cellular components and accelerates senescence, and how this response applies to variation in animal performance and longevity is postulated.

A mitohormetic response to pro-oxidant exposure in the house mouse.

These data provide the first chronological description of the mitohormetic response after a mild dose of irradiation and highlight the protective response that cells display to ROS exposure.

References

SHOWING 1-10 OF 182 REFERENCES

Radiation-induced autophagy in normal and cancer cells: Towards novel cytoprotection and radio-sensitization policies?

Radiobiology research should focus on the differential effect of fractionation on the induction of autophagy in different tumors and on the manipulation of this with autophophagy triggering agents, and the role of pretreatment autophagic indices in tumor cells in predicting radiotherapy and chemotherapy outcome should be examined.

Metabolic oxidation/reduction reactions and cellular responses to ionizing radiation: A unifying concept in stress response biology

Evidence supporting the concept that perturbations in intracellular metabolic oxidation/reduction reactions contribute to the biological effects of radiation exposure is focused on as well as new concepts emerging from the field of free radical biology that may be relevant to future studies in radiobiology.

Regulation of autophagy by reactive oxygen species (ROS): implications for cancer progression and treatment.

An overview of the roles ROS and autophagy play in cell survival and cell death, and their importance to cancer is given.

Pathways that Regulate Autophagy and their Role in Mediating Tumor Response to Treatment

Radiation-induced inactivation of mTOR pathway was detrimental to cell survival and was associated with reversal of mitochondrial ATPase activity and mitochondrial hyperpolarization, decreased level of eukaryotic initiation factor 4G (eIF4G) and increased phosphorylation of p53.

ROS-mediated mechanisms of autophagy stimulation and their relevance in cancer therapy

The role of autophagy in cancer cells responding to ROS-producing agents, which are utilized as a therapeutic modality to kill cancer cells are focused on.

Evidence for beneficial low level radiation effects and radiation hormesis.

The linear-no-threshold (LNT) hypothesis for cancer risk is scientifically unfounded and appears to be invalid in favour of a threshold or hormesis, consistent with data both from animal studies and human epidemiological observations on low-dose induced cancer.

Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity.

Radioadaptive response revisited

Although adaptive response seems to function by an on/off principle, it is a phenomenon showing a high degree of inter- and intraindividual variability, it remains to be seen to what extent adaptive response is functional in humans at relevant dose and dose-rate exposures.

Mechanism of radiation‐induced bystander effects: a unifying model

Bystander observations imply that the relevant target for various radiobiological endpoints is larger than an individual cell, and a better understanding of the cellular and molecular mechanisms of the bystander phenomenon will allow a more accurate model for assessing the health effects of low doses of ionizing radiation.

Adaptive response and the influence of ageing: effects of low-dose irradiation on cell growth of cultured glial cells

The results indicated that PKC, ATM, DNAPK and/or P13K were involved in RAR for growth and BrdU incorporation of cultured glial cells and RAR decreased with ageing.
...