Low-dose radiotherapy effects the progression of anti-tumor response

Cellular senescence refers to the permanent arrest of cell cycle caused by intrinsic and/or extrinsic stressors including oncogene activation, irradiation, DNA damage, oxidative stress, and certain cytokines (including senescence associated secretory phenotype). Cellular senescence is an important factor in aging. Accumulation of senescent cells has been implicated in the causation of various age-related organ disorders, tissue dysfunction, and chronic diseases. It is widely accepted that the biological effects triggered by low-dose radiation (LDR) are different from those caused by high-dose radiation. Experimental evidence suggests that LDR may promote growth and development, enhance longevity, induce embryo production, and delay the progression of chronic diseases. The underlying mechanisms of these effects include modulation of immune response, stimulation of hematopoietic system, antioxidative effect, reduced DNA damage and improved ability for DNA damage repair. In this review, we discuss the possible mechanisms by which LDR prevents senescence and aging from the perspectives of inhibiting cellular senescence and promoting the removal of senescent cells. We review a wide broad of evidence about the beneficial impact of LDR in senescence and aging models (including cardiovascular diseases, neurological diseases, arthritis and osteoporosis, chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis) to highlight the potential value of LDR in preventing aging and age-related diseases. However, there is no consensus on the effect of LDR on human health, and several important aspects require further investigation. 

Role of low-dose radiation in senescence and aging: A beneficial perspective.

Radioactive contaminants create problems all over world, involving marine ecosystems, with their ecological importance increasing in the future. The review focuses on bioeffects of a series of alpha and beta emitting radioisotopes (americium-241, uranium-(235 + 238), thorium-232, and tritium) and gamma radiation. Low-intensity exposures are under special consideration. Great attention has been paid to luminous marine bacteria as representatives of marine microorganisms and a conventional bioassay system. This bioassay uses bacterial bioluminescence intensity as the main testing physiological parameter; currently, it is widely applied due to its simplicity and sensitivity. Dependences of the bacterial luminescence response on the exposure time and irradiation intensity were reviewed, and applicability of hormetic or threshold models was discussed. A number of aspects of molecular intracellular processes under exposure to low-intensity radiation were analyzed: (a) changes in the rates of enzymatic processes in bacteria with the bioluminescent system of coupled enzymatic reactions of NADH:FMN-oxidoreductase and bacterial luciferase taken as an example; (b) consumption of an intracellular reducer, NADH; (c) active role of reactive oxygen species; (d) repairing of the DNA damage. The results presented confirm the function of humic substances as natural radioprotectors.

/pdf/marine-bacteria-under-low-intensity-radioactive-exposure-1a139bvf.pdf

Marine Bacteria under Low-Intensity Radioactive Exposure: Model Experiments

Successful clinical methods for tumor elimination include a combination of surgical resection, radiotherapy, and chemotherapy. Radiotherapy is one of the crucial components of the cancer treatment regimens which allow to extend patient life expectancy. Current cutting-edge radiotherapy research is focused on the identification of methods that should increase cancer cell sensitivity to radiation and activate anti-cancer immunity mechanisms. Radiation treatment activates various cells of the tumor microenvironment (TME) and impacts tumor growth, angiogenesis, and anti-cancer immunity. Radiotherapy was shown to regulate signaling and anti-cancer functions of various TME immune and vasculature cell components, including tumor-associated macrophages, dendritic cells, endothelial cells, cancer-associated fibroblasts (CAFs), natural killers, and other T cell subsets. Dual effects of radiation, including metastasis-promoting effects and activation of oxidative stress, have been detected, suggesting that radiotherapy triggers heterogeneous targets. In this review, we critically discuss the activation of TME and angiogenesis during radiotherapy which is used to strengthen the effects of novel immunotherapy. Intracellular, genetic, and epigenetic mechanisms of signaling and clinical manipulations of immune responses and oxidative stress by radiotherapy are accented. Current findings indicate that radiotherapy should be considered as a supporting instrument for immunotherapy to limit the cancer-promoting effects of TME. To increase cancer-free survival rates, it is recommended to combine personalized radiation therapy methods with TME-targeting drugs, including immune checkpoint inhibitors.

Dual effects of radiotherapy on tumor microenvironment and its contribution towards the development of resistance to immunotherapy in gastrointestinal and thoracic cancers

Car-borne survey and dose assessment from external radiation exposure in Bangka Island.

The Linear-No-Threshold (LNT) model predicts a dose-dependent linear increase in cancer risk. This has been supported by biological and epidemiological studies at high-dose exposures. However, at low-doses (LDR ≤ 0.1 Gy), the effects are more elusive and demonstrate a deviation from linearity. In this study, the effects of LDR on the development and progression of mammary cancer in FVB/N-Tg(MMTVneu)202Mul/J mice were investigated. Animals were chronically exposed to total doses of 10, 100, and 2000 mGy via tritiated drinking water, and were assessed at 3.5, 6, and 8 months of age. Results indicated an increased proportion of NK cells in various organs of LDR exposed mice. LDR significantly influenced NK and T cell function and activation, despite diminishing cell proliferation. Notably, the expression of NKG2D receptor on NK cells was dramatically reduced at 3.5 months but was upregulated at later time-points, while the expression of NKG2D ligand followed the opposite trend, with an increase at 3.5 months and a decrease thereafter. No noticeable impact was observed on mammary cancer development, as measured by tumor load. Our results demonstrated that LDR significantly influenced the proportion, proliferation, activation, and function of immune cells. Importantly, to the best of our knowledge, this is the first report demonstrating that LDR modulates the cross-talk between the NKG2D receptor and its ligands.

Effects of Chronic Low-Dose Internal Radiation on Immune-Stimulatory Responses in Mice.

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Effects of Chronic Low-Dose Internal Radiation on Immune-Stimulatory Responses in Mice.