Radiation-induced bystander effect on the brain after fractionated spinal cord irradiation of aging rats.

We investigated the influence of the so-called bystander effect on metabolic and histopathological changes in the rat brain after fractionated spinal cord irradiation. The study was initiated with adult Wistar male rats (n = 20) at the age of 9 months. The group designated to irradiation (n = 10) and the age-matched control animals (n = 10) were subjected to an initial measurement using in vivo proton magnetic resonance spectroscopy (1H MRS) and magnetic resonance imaging (MRI). After allowing the animals to survive until 12 months, they received fractionated spinal cord irradiation with a total dose of 24 Gy administered in 3 fractions (8 Gy per fraction) once a week on the same day for 3 consecutive weeks. 1H MRS and MRI of brain metabolites were performed in the hippocampus, corpus striatum, and olfactory bulb (OB) before irradiation (9-month-old rats) and subsequently 48 h (12-month-old) and 2 months (14-month-old) after the completion of irradiation. After the animals were sacrificed at the age of 14 months, brain tissue changes were investigated in two neurogenic regions: the hippocampal dentate gyrus (DG) and the rostral migratory stream (RMS). By comparing the group of 9-month-old rats and individuals measured 48 h (at the age of 12 months) after irradiation, we found a significant decrease in the ratio of total N-acetyl aspartate to total creatine (tNAA/tCr) and gamma-aminobutyric acid to tCr (GABA/tCr) in OB and hippocampus. A significant increase in myoinositol to tCr (mIns/tCr) in the OB persisted up to 14 months of age. Proton nuclear magnetic resonance (1H NMR)-based plasma metabolomics showed a significant increase in keto acids and decreased tyrosine and tricarboxylic cycle enzymes. Morphometric analysis of neurogenic regions of 14-month-old rats showed well-preserved stem cells, neuroblasts, and increased neurodegeneration. The radiation-induced bystander effect more significantly affected metabolite concentration than the distribution of selected cell types.

The Biological Process of Aging and the Impact of Ionizing Radiation.

Ionizing radiation is used to create models of accelerated aging because the processes of aging and radiation injury share common elements. In this chapter we review the biological processes of aging and the similarities and impact of ionizing radiation on those processes. The information draws on data from laboratory studies and from epidemiology studies of radiation exposure victims. The chapter reviews the effects of radiation on DNA, cells, and organs systems on aged adults. The science of aging and the effect of radiation on the aging process are areas of active research and our understanding is evolving.

The response of bioactive titanium surfaces with different structure to UVC-irradiation to eliminate the negative effect on biological properties during aging time.

The biological aging of titanium implants affects the service lifetime negatively in clinical applications, and Ultraviolet (UV) irradiation is an applicable method to overcome the biological aging. This study investigated the changes in surface characteristics and biological properties of bioactive titanium surfaces with different structure and topography after Ultraviolet C (UVC) irradiation. The bioactive titanium surfaces were prepared by anodizing (AO), sandblasting and acid-etching (SLA), acid-alkali etching (AA), alkali-heat etching (AH) methods. Samples were stored at dark for 7 weeks to simulate biological aging process and then irradiated by UVC for 2 h. The results showed that the hydroxyl groups (Ti-OH) on surfaces, which are crucial to enhance the biological properties, were easier to be generated on AO surfaces by UVC-irradiation, owing to a mixture of anatase and rutile on surfaces. UVC-irradiation had the strongest effect on AO surfaces to enhance the bioactivity in bone-like apatite deposition and better biocompatibility in mesenchymal stem cells (MSCs) attachment and proliferation. Therefore, titanium surfaces with a mixture phase of anatase and rutile have the potential to effectively utilize the benefits of UVC-irradiation to overcome the negative effects of the biological aging and have a promising clinical application prospect.

AGING OF THE CHORNOBYL CATASTROPHE SURVIVORS AND PROBLEMS OF THEIR MENTAL HEALTH SURVEY. / STARINNIa POSTRAZhDALYKh VNASLIDOK ChORNOBYL'S'KOÏ KATASTROFY TA PROBLEMY DOSLIDZhENNIa ÏKhN'OGO PSYKhIChNOGO ZDOROV'Ia.

BACKGROUND: Depopulation processes in Ukraine have been affected by the Chornobyl catastrophe (ChC), but therate of demographic aging of survivors remains uncertain. Although the mental health disorders of the survivors arerecognized internationally, problems of their research remain unresolved. Thus, these areas of research are relevant.Objective is to determine the rate of demographic aging of survivors of the Chornobyl NPP (ChNPP) accident and toanalyze the state of their mental health survey, outlining solutions. MATERIALS AND METHODS: Information and statistical sources for 1986-2019 of the Ministry of Health of Ukraine andthe State Statistics Service of Ukraine on the age of the ChC survivors are used. The results of previous own researchand other scientists using the data of the Clinical and Epidemiological Register (CER) of the State Institution«National Research Center for Radiation Medicine of the National Academy of Medical Sciences of Ukraine¼(NRCRM), the State Register of ChC survivors (SRU), and the Department of Radiation Psychoneurology, Institute ofClinical Radiology, NRCRM are integrated. Theoretical, general scientific, demographic and mathematical-statisticalresearch methods and documentary analysis are used. RESULTS: It is shown that in 2018, compared to 1995, the number of the ChC survivors, who are under the supervi-sion of the Ministry of Health of Ukraine, decreased by almost 987 thousand. The part of people born from personsof the 1st-3rd accounting groups increased in the structure of survivors (from 13.1 % in 1995 to 13.6 %), and thisdecreased in persons living or lived in the territories subject to supervision (75.1 % and 63.1 %, respectively), butin evacuees and Chornobyl clean-up workers (liquidators) this did not change significantly. A high level of aging ofthe ChC survivors (except for the 4th group) is revealed: liquidators - 59.0 %; evacuees - 25.0 %, and residents ofradioactively contaminated territories (RCT) - 30.7 %. It has been proved that the countries of RCT differ signifi-cantly in the number of the ChC survivors and their structure. The increase in the post-accident period indicators ofthe level of aging and the average age of the RCT population indicates negative changes in age parameters and theneed to continue research to identify factors «responsible¼ for such changes. Long-term mental health disordersand neuropsychiatric effects in the ChC survivors have been identified - an excess of cerebrovascular pathology andneurocognitive deficits, especially in liquidators, which may indicate an accelerated aging. Radiation risks havebeen revealed for acute and chronic cerebrovascular pathology and organic mental disorders of non-psychotic andpsychotic levels. Neurophysiological and molecular-biological atypia of aging processes under an exposure to lowdoses of and low dose rate of ionizing radiation have been found. The psyche under the age of 40 years old at thetime of exposure is more vulnerable. Existing statistical and registry data underestimate the level of mental disor-ders in the population of Ukraine, including the ChC survivors by an order of magnitude. CONCLUSIONS: The ChC survivors are aging in the country. The negative tendencies in age parameters of survival indi-cate the need to continue research to identify the factors «responsible¼ for such changes. Mental health disordersand neuropsychiatric effects in the ChC survivors are underestimated. It is necessary to create a national psychiatricregistry of Ukraine and long-term (lifelong) monitoring of survivors with well-planned clinical and epidemiologicalstudies of general and mental health with reliable dosimetric support based on national registries using the latest information technologies.

Exposure to ionizing radiation disrupts normal epigenetic aging in Japanese medaka.

Alterations to the epigenome are a hallmark of biological aging and age-dependent patterning of the DNA methylome ("epigenetic aging") can be modeled to produce epigenetic age predictors. Rates of epigenetic aging vary amongst individuals and correlate to the onset of age-related disease and all-cause mortality. Yet, the origins of epigenetic-to-chronological age discordance are not empirically resolved. Here, we investigate the relationship between aging, DNA methylation, and environmental exposures in Japanese medaka (Oryzias latipes). We find age-associated DNA methylation patterning enriched in genomic regions of low CpG density and that, similar to mammals, most age-related changes occur during early life. We construct an epigenetic clock capable of predicting chronological age with a mean error of 61.1 days (~8.4% of average lifespan). To test the role of environmental factors in driving epigenetic age variation, we exposed medaka to chronic, environmentally relevant doses of ionizing radiation. Because most organisms share an evolutionary history with ionizing radiation, we hypothesized that exposure would reveal fundamental insights into environment-by-epigenetic aging interactions. Radiation exposure disrupted epigenetic aging by accelerating and decelerating normal age-associated patterning and was most pronounced in cytosines that were moderately associated with age. These findings empirically demonstrate the role of DNA methylation in integrating environmental factors into aging trajectories.

Ultraviolet radiation protection potentials of Methylene Blue for human skin and coral reef health.

Methylene blue (MB) is a century-old medicine, a laboratory dye, and recently shown as a premier antioxidant that combats ROS-induced cellular aging in human skins. Given MB's molecular structure and light absorption properties, we hypothesize that MB has the potential to be considered as a sunscreen active for UV radiation protection. In this study, we tested the effects of MB on UVB ray-induced DNA double-strand breaks in primary human keratinocytes. We found that MB treatment reduced DNA damages caused by UVB irradiation and subsequent cell death. Next, we compared MB with Oxybenzone, which is the most commonly used chemical active ingredient in sunscreens but recently proven to be hazardous to aquatic ecosystems, in particular to coral reefs. At the same concentrations, MB showed more effective UVB absorption ability than Oxybenzone and significantly outperformed Oxybenzone in the prevention of UVB-induced DNA damage and the clearance of UVA-induced cellular ROS. Furthermore, unlike Oxybenzone, MB-containing seawater did not affect the growth of the coral species Xenia umbellata. Altogether, our study suggests that MB has the potential to be a coral reef-friendly sunscreen active ingredient that can provide broad-spectrum protection against UVA and UVB.

Impact of aging on gene expression response to x-ray irradiation using mouse blood.

As a radiation biodosimetry tool, gene expression profiling is being developed using mouse and human peripheral blood models. The impact of dose, dose-rate, and radiation quality has been studied with the goal of predicting radiological tissue injury. In this study, we determined the impact of aging on the gene expression profile of blood from mice exposed to radiation. Young (2 mo) and old (21 mo) male mice were irradiated with 4 Gy x-rays, total RNA was isolated from whole blood 24 h later, and subjected to whole genome microarray analysis. Pathway analysis of differentially expressed genes revealed young mice responded to x-ray exposure by significantly upregulating pathways involved in apoptosis and phagocytosis, a process that eliminates apoptotic cells and preserves tissue homeostasis. In contrast, the functional annotation of senescence was overrepresented among differentially expressed genes from irradiated old mice without enrichment of phagocytosis pathways. Pathways associated with hematologic malignancies were enriched in irradiated old mice compared with irradiated young mice. The fibroblast growth factor signaling pathway was underrepresented in older mice under basal conditions. Similarly, brain-related functions were underrepresented in unirradiated old mice. Thus, age-dependent gene expression differences should be considered when developing gene signatures for use in radiation biodosimetry.

Age and insulin-like growth factor-1 impact PCNA monoubiquitination in UVB-irradiated human skin.

Nonmelanoma skin cancers occur primarily in individuals over the age of 60 and are characterized by an abundance of ultraviolet (UV) signature mutations in keratinocyte DNA. Though geriatric skin removes UV photoproducts from DNA less efficiently than young adult skin, it is not known whether the utilization of other prosurvival but potentially mutagenic DNA damage tolerance systems such as translesion synthesis (TLS) is altered in older individuals. Using monoubiquitination of the replicative DNA polymerase clamp protein PCNA (proliferating cell nuclear antigen) as a biochemical marker of TLS pathway activation, we find that UVB exposure of the skin of individuals over the age of 65 results in a higher level of PCNA monoubiquitination than in the skin of young adults. Furthermore, based on previous reports showing a role for deficient insulin-like growth factor-1 (IGF-1) signaling in altered UVB DNA damage responses in geriatric human skin, we find that both pharmacological inhibition of the IGF-1 receptor (IGF-1R) and deprivation of IGF-1 potentiate UVB-induced PCNA monoubiquitination in both human skin ex vivo and keratinocytes in vitro. Interestingly, though the TLS DNA polymerase Pol eta can accurately replicate the major photoproducts induced in DNA by UV radiation, we find that it fails to accumulate on chromatin in the absence of IGF-1R signaling and that this phenotype is correlated with increased mutagenesis in keratinocytes in vitro. Thus, altered IGF-1/IGF-1R signaling in geriatric skin may predispose epidermal keratinocytes to carry out a more mutagenic form of DNA synthesis following UVB exposure.

Low-grade chronic inflammation and immune alterations in childhood and adolescent cancer survivors: A contribution to accelerated aging?

BACKGROUND: The long-term consequences of chemotherapy and radiotherapy result in a high prevalence and early onset of age-related chronic diseases in survivors. We aimed to examine whether childhood and adolescent cancer survivors (CS) demonstrate biomarkers of accelerated aging. METHODS: We evaluated 50 young adult CS at 11 [8-15] years after cancer diagnosis, and 30 healthy, age and sex-matched controls, who were unexposed to cancer therapy. Using a machine-learning approach, we assessed factors discriminating CS from controls and compared selected biomarkers and lymphocyte subpopulations with data from the Framingham Heart Study (FHS) cohort and the Genotype Tissue Expression (GTEx) project. RESULTS: Survivors compared with controls had higher levels of C-reactive protein and fibrinogen. The surface expression of CD38 on T cells was increased, and there was an increase in the percentage of memory T cells in survivors, compared with the unexposed group. The relationships between above cell subpopulations and age were consistent in CS, FHS, and GTEx cohorts, but not in controls. CONCLUSIONS: Young pediatric cancer survivors differ from age-related controls in terms of activation of the adaptive immune system and chronic, low-grade inflammation. These changes resemble aging phenotype observed in older population. Further research in biomarkers of aging in young, adult childhood cancer survivors is warranted, as it may facilitate screening and prevention of comorbidities in this population.

Twins, Telomeres, and Aging-in Space!

BACKGROUND: The landmark National Aeronautics and Space Administration Twins Study represented an integrated effort to launch human space life science research into the modern age of molecular- and "omics"-based studies. As part of the first One-Year Mission aboard the International Space Station, identical twin astronauts Scott and Mark Kelly were the subjects of this "out of this world" research opportunity. Telomeres, the natural ends of chromosomes that shorten with cell division and a host of lifestyle factors and stresses, are key molecular determinants of aging and aging trajectories. METHODS: We proposed that telomere length dynamics (changes over time) represent a particularly relevant and integrative biomarker for astronauts, as they reflect the combined experiences and environmental exposures encountered during spaceflight. Telomere length (quantitative polymerase chain reaction and telomere fluorescence in situ hybridization) and telomerase activity (quantitative polymerase chain reaction -telomere repeat amplification protocol) were longitudinally assessed in the space- and earth-bound twins. Chromosome aberrations (directional genomic hybridization), signatures of radiation exposure, were also evaluated. RESULTS: The twins had relatively similar telomere lengths before spaceflight, and the earth-bound twins' telomeres remained relatively stable over the course of the study. Surprisingly, the space twins' telomeres were longer during spaceflight, and upon return to Earth shortened rapidly, resulting in many more short telomeres after spaceflight than before. Chromosomal signatures of space radiation exposure were also elevated during spaceflight, and increased inversion frequencies persisted after spaceflight, suggestive of ongoing genome instability. CONCLUSION: Although the definitive mechanisms underlying such dramatic spaceflight-associated shifts in telomere length remain unclear, improved maintenance of telomere length has important implications for aging science and improving healthspan for those on Earth, as well.

Optically Improved Mitochondrial Function Redeems Aged Human Visual Decline.

The age spectrum of human populations is shifting toward the older with larger proportions suffering physical decline. Mitochondria influence the pace of aging as the energy they provide for cellular function in the form of adenosine triphosphate (ATP) declines with age. Mitochondrial density is greatest in photoreceptors, particularly cones that have high energy demands and mediate color vision. Hence, the retina ages faster than other organs, with a 70% ATP reduction over life and a significant decline in photoreceptor function. Mitochondria have specific light absorbance characteristics influencing their performance. Longer wavelengths spanning 650->1,000 nm improve mitochondrial complex activity, membrane potential, and ATP production. Here, we use 670-nm light to improve photoreceptor performance and measure this psychophysically in those aged 28-72 years. Rod and cone performance declined significantly after approximately 40 years of age. 670-nm light had no impact in younger individuals, but in those around 40 years and older, significant improvements were obtained in color contrast sensitivity for the blue visual axis (tritan) known to display mitochondrial vulnerability. The red visual axis (protan) improved but not significantly. Rod thresholds also improved significantly in those >40 years. Using specific wavelengths to enhance mitochondrial performance will be significant in moderating the aging process in this metabolically demanding tissue.

The age-dependent effect of high-dose X-ray radiation on NFκB signaling, structure, and mechanical behavior of the intervertebral disc.

Purpose: Ionizing radiation damages tissue and provokes inflammatory responses in multiple organ systems. We investigated the effects of high-dose X-ray radiation on the molecular inflammation and mechanical function of the intervertebral disc (IVD).Methods: Functional spine units (FSUs) containing the vertebrae-IVDs-vertebrae structure extracted from 1-month, 6-month, and 16-month-old NFκB-luciferase reporter mice and from 6-month-old myeloid differentiation factor 88 (MyD88)-null mice. After a preconditioning period in culture, the FSUs were subjected a single dose of ionizing X-ray radiation at 20 Gys, and then NFκB expression was monitored. The IVDs were then subjected to mechanical testing using dynamic compression, glycosaminoglycan (GAG) quantification, and histological analyses.Results: In the 1-month-old FSUs, the NFκB-driven luciferase activity was significantly elevated for 1 day following the exposure to radiation. The 6-month-old FSUs showed increased NFκB activity for 3 days, while the 16-month-old FSUs sustained elevated levels of NFκB activity throughout the 10-day culture period. All irradiated groups showed significant loss of disc height, GAG content, mechanical function and changes in structure. Ablation of MyD88 blunted the radiation-mediated NFκB signaling, and preserved GAG content, and the IVDs' structure and mechanical performance.Conclusions: These results suggest that high-dose radiation affects the IVDs' NFκB-dependent inflammatory processes that subsequently lead to functional deterioration. Blocking the transactivation potential of NFκB via MyD88 ablation preserved the structure and mechanical function of the FSUs. The long-term effects of radiation on IVD homeostasis should be considered in individuals susceptible to occupational and medical exposure.

Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans.

The biological effects of magnetic fields are a research hotspot in the field of biomedical engineering. In this study, we further investigated the effects of a rotating magnetic field (RMF; 0.2 T, 4 Hz) on the growth of human umbilical vein endothelial cells (HUVECs) and Caenorhabditis elegans. The results showed that RMF exposure prolonged the lifespan of C. elegans and slowed the aging of HUVECs. RMF treatment of HUVECs showed that activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) was associated with decreased mitochondrial membrane potential (MMP) due to increased intracellular Ca2+ concentrations induced by endoplasmic reticulum stress in anti-aging mechanisms. RMF also promoted the health status of C. elegans by improving activity, reducing age-related pigment accumulation, delaying Aß-induced paralysis and increasing resistance to heat and oxidative stress. The prolonged lifespan of C. elegans was associated with decreased levels of daf-16 which related to the insulin/insulin-like growth factor signaling pathway (IIS) activity and reactive oxygen species (ROS), whereas the heat shock transcription factor-1 (hsf-1) pathway was not involved. Moreover, the level of autophagy was increased after RMF treatment. These findings expand our understanding of the potential mechanisms by which RMF treatment prolongs lifespan.

lncRNA H19 contributes to oxidative damage repair in the early age-related cataract by regulating miR-29a/TDG axis.

Age-related cataract (ARC) is caused by the exposure of the lens to UVB which promotes oxidative damage and cell death. This study aimed to explore the role of lncRNA H19 in oxidative damage repair in early ARC. lncRNAs sequencing technique was used to identify different lncRNAs in the lens of early ARC patients. Human lens epithelial cells (HLECs) were exposed to ultraviolet irradiation; and 8-OHdG ELISA, Cell counting kit 8 (CCK8), EDU, flow cytometry and TUNEL assays were used to detect DNA damage, cell viability, proliferation and apoptosis. Luciferase assay was used to examine the interaction among H19, miR-29a and thymine DNA glycosylase (TDG) 3'UTR. We found that lncRNA H19 and TDG were highly expressed while miR-29a was down-regulated in the three types of early ARC and HLECs exposed to ultraviolet irradiation, compared to respective controls. lncRNA H19 knockdown aggravated oxidative damage, reduced cell viability and proliferation, and promoted apoptosis in HLECs, while lncRNA H19 overexpression led to opposite effects in HLECs. Mechanistically, miR-29a bound TDG 3'UTR to repress TDG expression. lncRNA H19 up-regulated the expression of TDG by repressing miR-29a because it acted as ceRNA through sponging miR-29a. In conclusion, the interaction among lncRNA H19, miR-29a and TDG is involved in early ARC. lncRNA H19 could be a useful marker of early ARC and oxidative damage repair pathway of lncRNA H19/miR-29a/TDG may be a promising target for the treatment of ARC.

'Stemness' and 'senescence' related escape pathways are dose dependent in lung cancer cells surviving post irradiation.

AIMS: Lung cancer is one of the main causes of cancer-related deaths worldwide and radiotherapy is a major treatment of choice. However, radioresistance is a main reason for radiotherapy failure or tumor relapse. Here, we investigated possible mechanisms associated with cancer cell radioresistance. MATERIALS AND METHODS: We compared two newly derived cell lines, namely A549-IR3 and A549-IR6, which survived repeated (3 or 6 times) 4 Gy exposure of parental A549 lung cancer cell line. DNA repair ability, stemness and senescence were comparatively studied. KEY FINDINGS: A549-IR3 exhibited higher proliferation ability and radioresistance compared to parental and A549-IR6 cells. Enhanced radioresistance was not accompanied by chemoresistance to cisplatin or docetaxel. DNA repair kinetics (γΗ2ΑΧ expression) were similar in all cell lines. A549-IR3 cells exhibited a significant rise in stem cell markers (CD44, CD133, OCT4, SOX2 and NANOG) whereas A549-IR6 displayed an increased senescent population. SIGNIFICANCE: Cancer cells surviving after radiotherapy may follow two different escape pathways: selection for radioresistance resulting in regrowth, and in clinical terms relapse, or above an irradiation threshold, stem-cells die and cancer cells become senescent, leading the tumor to a state of dormancy.

Cataractogenic load - A concept to study the contribution of ionizing radiation to accelerated aging in the eye lens.

Ionizing radiation (IR) damages DNA and other macromolecules, including proteins and lipids. Most cell types can repair DNA damage and cycle continuously their macromolecules as a mechanism to remove defective proteins and lipids. In those cells that lack nuclei and other organelles, such as lens fiber cells and mammalian erythrocytes, IR-induced damage to macromolecules is retained because they cannot be easily replenished. Whilst the life span for an erythrocyte is several months, the life span of a human lens is decades. There is very limited turnover in lens macromolecules, therefore the aging process greatly impacts lens structure and function over its lifetime. The lens is a tissue where biomolecular longevity, lifelong retention of its components and continued growth are integral to its homeostasis. These characteristics make the lens an excellent model to study the contribution of retained macromolecular damage over time. Epidemiological data have revealed a significant association between exposure to IR, the loss of lens optical function and the formation of cataracts (cataractogenesis) later in life. Lifestyle, genetic and environmental factors all contribute to cataractogenesis due to their effect on the aging process. Cataract is an iconic age-related disease in humans. IR is a recognised cause of cataract and the occupational lens dose limit is reduced from 150 to 20 mGy / year averaged over 5 years (ICRP Publication 118). Understanding the effects of low dose IR on the lens and its role in cataractogenesis is therefore very important. So we redefine "cataractogenic load" as a term to account for the combined lifestyle, genetic and environmental processes that increase biomolecular damage to lens macromolecules leading to cataract formation. These processes weaken metabolic defenses, increase post-translational protein modifications, and alter the lipid structure and content of the lens. IR exposure is a significant insult to the lens because of free radical generation and the ensuing oxidative stress. We support the concept that damage caused by IR compounds the aging process by increasing the cataractogenic load, hereby accelerating lens aging and its loss of function.

Replicative and radiation-induced aging: a comparison of gene expression profiles.

All living organisms are subject to the aging process and experience the effect of ionizing radiation throughout their life. There have been a number of studies that linked ionizing radiation process to accelerated aging, but comprehensive signalome analysis of both processes was rarely conducted. Here we present a comparative signaling pathway based analysis of the transcriptomes of fibroblasts irradiated with different doses of ionizing radiation, replicatively aged fibroblasts and fibroblasts collected from young, middle age and old patients. We demonstrate a significant concordance between irradiation-induced and replicative senescence signalome signatures of fibroblasts. Additionally, significant differences in transcriptional response were also observed between fibroblasts irradiated with high and low dose. Our data shows that the transcriptome of replicatively aged fibroblasts is more similar to the transcriptome of the cells irradiated with 2 Gy, than with 5 сGy.This work revealed a number of signaling pathways that are shared between senescence and irradiation processes and can potentially be targeted by the new generation of gero- and radioprotectors.

Chronic exposure to gamma irradiation at low-dose rates accelerates blood pressure decline associated with aging in female B6C3F1 mice.

PURPOSE: Many studies are focusing on the biological effects of gamma irradiation at low-dose rates. Studies have shown that chronic exposure to gamma irradiation at low-dose rates shortened the lifespan of mice due to neoplasm formation. The aim of this study was to clarify the physiological effects of long-term exposure to gamma irradiation at low-dose rates in mice, measured with noninvasive parameters such as blood pressure. MATERIALS AND METHODS: Specific-pathogen-free female B6C3F1 mice were irradiated with gamma rays at a low dose of 20 mGy/day - a dose rate shown to shorten the life span in previous studies. The blood pressure parameters (systolic, diastolic, and mean blood pressure), heart rate, tail blood volume, and blood flow of the mice were measured every 7 weeks. Age-matched, non-irradiated mice were used as controls. RESULTS AND CONCLUSION: The blood pressure levels of the irradiated mice decreased at an earlier age compared to the non-irradiated control mice. The expression levels of the marker genes of aging that are also associated with regulation of blood pressure showed significant differences between non-irradiated and irradiated mice. These results indicated that long-term exposure to gamma irradiation at low-dose rates induce the expression levels of Rap1a and reduces Panx1 and Sirt3, which may have contributed to the accelerated blood pressure decline in female mice.

Photodynamic and photobiological effects of light-emitting diode (LED) therapy in dermatological disease: an update.

Benefit deriving from the use of light is known since ancient time, but, only in the last decades of twentieth century, we witnessed the rapid expansion of knowledge and techniques. Light-emitted diode (LED)-based devices represent the emerging and safest tool for the treatment of many conditions such as skin inflammatory conditions, aging, and disorders linked to hair growth. The present work reviews the current knowledge about LED-based therapeutic approaches in different skin and hair disorders. LED therapy represents the emerging and safest tool for the treatment of many conditions such as skin inflammatory conditions, aging, and disorders linked to hair growth. The use of LED in the treatment of such conditions has now entered common practice among dermatologists. Additional controlled studies are still needed to corroborate the efficacy of such kind of treatment.