Mitochondria and radiation sensitivity of cells

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by
Univ. of Rochester Atomic Energy Project , Rochester, N.Y
Mitochondria, Radiation -- Physiological e
Statementby E. Tsinga, G.W. Casarett.
SeriesTID -- 4500., AEC Research and development report -- Ur-666., AEC research and development report -- Ur-666.
ContributionsCassarett, George William, 1920-, University of Rochester. Atomic Energy Project.
The Physical Object
Paginationiii, 59 p., [13] leaves of plates :
ID Numbers
Open LibraryOL17614695M
OCLC/WorldCa36777441

Abstract "Contract Weng between the U.S. Atomic Energy Commission and the University of Rochester, administered by the Department of Radiation Biology and Biophysics of the School of Medicine and Dentistry."Some of the pages numbered as leaves."Unclassified.""Date completed: 4/13/65 ; Date of issue: 7/19/""UC ; Biology and Medicine ; TID (41st Ed.).""UR"Includes.

Description Mitochondria and radiation sensitivity of cells PDF

Immo E. Scheffler, PhD, is Professor in the Division of Biology at the University of California, San addition to this well-received book, Dr. Scheffler has more than original publications in scientific literature and has written numerous book chapters. When cells undergo apoptosis, a series of key events occur in mitochondria, including down-regulating the ratio of the apoptosis-related protein Bax /Bcl-2 can change the permeability of mitochondrial membranes, which lead to the release of cytochrome c from mitochondria into the cytosol, and then activate the caspase cascade (Vakifahmetoglu Cited by: 4.

Mitochondria in radiation research 4 Could mitochondria be targets of radiation. 5 Radiation-induced cell death 15 Mitochondrial dynamics and apoptosis 16 Evidence for modulation of sensitivity to radiation and other cytotoxic agents by. More mitochondria and cytoskeleton were found in irradiated cells compared (figure 4(b)) to non-irradiated cells (figure 4(a)).

MTT is reduced to purple formazen by the dehydrogenase enzymes in the mitochondria of living cells (MosmannLiu et alBerridge and Tan ) and the production of formazan is proportional to the level of Cited by: Under physiological conditions, nitric oxide (NO) produced by the endothelial NO synthase (eNOS) upregulates hepatic insulin sensitivity.

Recently, contact sites between the endoplasmic reticulum and mitochondria named mitochondria-associated membranes (MAMs) emerged as a crucial hub for insulin signaling in the liver. As mitochondria are targets of NO, we explored whether NO regulates.

Details Mitochondria and radiation sensitivity of cells FB2

Protocol 1 Isolation of Mitochondria from Tissue Culture Cells David A. Clayton1 and Gerald S. Shadel2,3,4 1JaneliaFarmResearchCampus,HowardHughesMedicalInstitute,Ashburn,Virginia;2Department ofPathology,YaleUniversitySchoolofMedicine,NewHaven,Connecticut;3DepartmentofGenetics, Yale University School of Medicine, New Haven, Connecticut Transient generation of reactive oxygen or nitrogen (ROS/RNS), detected with dihydrodichlorofluoroscein by fluorescence Mitochondria and radiation sensitivity of cells book, occurs within minutes of exposing cells to ionizing radiation.

In the 1–10 Gy dose range, the amount of ROS/RNS produced/cell is constant, but the percentage of producing cells increases with dose (20 to 80%). Reversible depolarization of the mitochondrial. After using mitochondria Complex I inhibitors, rotenone and metformin, to treat glioma cells, we found the resistant glioma cells re-sensitized to radiation.

These results demonstrate that Complex I is associated with the fractioned radiation-induced radioresistance of glioma and would be a potent target for clinical radiotherapy of glioma. Mitochondria are the organelles responsible for cellular energy production and numerous other cell functions and they are adversely affected by electromagnetic radiation in many inter-related ways.

Electromagnetic radiation causes structural damage to mitochondria. ROS and RNS production by mitochondria and cell membrane and, also, We neglected morphological or radiation sensitivity changes during proliferation (S-phase) as well as.

It is well documented in the models of isolated mitochondria and whole cells that monochromatic radiation in visible and IR‐A region can affect ΔΨ m and stimulate ATP synthesis. The illumination of isolated rat liver mitochondria increased ATP synthesis and the consumption of O 2 (29, 33, 34).

The hypoxia-inducible transcription factors (HIF)-1/2α are the main oxygen sensors which regulate the adaptation to intratumoral hypoxia. The aim of this study was to assess the role of the HIF proteins in regulating the radiation response of a non-small cell lung cancer (NSCLC) in vitro model.

To directly assess the unique and overlapping functions of HIF-1α and HIF-2α, we use. In other more recent studies, neural cell apoptosis in NGF-differentiated PC12 rat cells has been induced by microwave exposure via the mitochondria-dependent caspase-3 pathway.

It represents one of three cellular apoptotic pathways including the extrinsic death receptor-dependent pathway, the intrinsic mitochondria-dependent pathway, and the.

Increasing oxygenation and radiation sensitivity following photodynamic therapy with verteporfin in the RIF-1 tumor. Author(s): It was huypothesized that this mechanism arises from the reduced oxygen consumption from cells where the PDT has targeted the mitochondria and shut down cellular respiration.

Tumor blood flow was measured and found. Fluorescent Immunocytochemistry Staining for Mitochondria and Autophagy Markers. Cells were fixed 5 minutes after RF exposure with 2% paraformaldehyde overnight and then stained with Tom20 (F10) antibody (Santa Cruz Biotechnology, Inc., Dallas, TX) as a marker for mitochondria or anti‐LC3B antibody (Cell Signaling Technology, Danvers, MA) as.

Mitochondria play an essential role in cellular apoptosis, and are relevant to the chemoresistance of cancer cells. Furthermore, mitochondria are a major player in many cellular processes and are.

Mitochondrial targeting GS-nitroxides protect cells with increased numbers of mitochondria, which advantages normal cells (Figure (Figure2). Total bone marrow radiosensitivity in Fancd2 −/− mice might be explained based on the radiation sensitivity of stromal cells, but not hematopoietic cells.

Elliott, R.L., Jiang, X.P. and Head, J.F. () Mitochondria Organelle Transportation Introduction of Normal Epithelial Mitochondria into Human Cancer Cells Inhibits Proliferation and Increases Drug Sensitivity.

Breast Cancer Research and Treatment,Book. Advanced Search. Toggle navigation Dineen S, Kapur P, Saha D, Meyer J. Role of p53, Bax, p21, and DNA-PKcs in radiation sensitivity of HCT cells and xenografts. radiosensitization, inflammation, redox, fibrosis, tumor hypoxia, DNA repair, mitochondria, AMPK, tumor resistance, cell cycle.

Abstract:Background: Nowadays, ionizing. These data suggest that all anticancer effects of M/A result from a specific mechanism, tightly connected to the mitochondria of cancer cells. At low/tolerable doses of M/A (1// μ M/ μ M) attainable in cancer by oral and parenteral administration, M/A sensitized cancer cells to conventional anticancer drugs, exhibiting synergistic or.

threshold level critical for cell survival, whereas mitochon-dria in normal cells would still be able to produce enough ATP. However, further studies challenged this idea and revealed that tumor mitochondria do respire and produce ATP [4].

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Independent of whether mitochondrial respiration is low or not, cancer cells do exhibit high rates of. Dose-independent generation of HNE in H/wtp53 cells irradiated with keV radiation. Cells were irradiated with Gy and Gy at keV and with Gy at keV.

Two hours after irradiation, the cells were fixed and immunofluorescence staining with an. III. Mitochondrial Metabolism and Cell Proliferation. The Warburg effect: The mitochondrial control of proliferation.

Mitochondria and redox control in normal and tumor cells. Stem cells, mitochondrial ROS metabolism, and differentiation.

ROS and mitochondrial malignancy: The example of p E. Another disadvantage is that some tumor cells are farther away from the site of radiation and hence might receive a lower intensity of the radiation beam.

Moreover, the cells can develop resistance to the radiation. Usually the sensitivity of the mitotically active tumor cells is only slightly higher than that of surrounding healthy tissue. The involvement of reactive oxygen species (ROS) from mitochondria (mtROS) in the cross-resistance to X-rays and DTX was studied.

Methods and Materials: Sensitivity to anticancer agents was determined by a modified high-density cell survival or water-soluble tetrazolium salt assay. DTX-induced mtROS generation was determined by MitoSOX red. Once the mitochondria of your cells use up the oxygen, carbon dioxide is released from your cells.

This carbon dioxide finds its way back to your lungs to be released into the air through exhalation. Cellular Energy Production. Your cells need energy for a variety of purposes, including DNA, RNA, cell division, and protein synthesis. Most importantly, treatment with the small-molecule, superoxide dismutase mimetic (GC; μmol/L) significantly mitigated the increased sensitivity of old fibroblasts to IR and chemotherapy and partially restored mitochondrial function without affecting IR or chemotherapy-induced cancer cell killing.

InGoldfeder first hypothesized that mitochondria play a role in radiosensitivity, based on the fact that cells with large numbers of mitochondria still function if irradiation compromises a substantial proportion of them.

Mitochondrial DNA appears to be more susceptible to damage by IR and chemically-induced oxidative stress. UV Radiation in Global Climate Change: Measurements, Modeling and Effects on Ecosystems Genetic (DNA) and Ultra-Structural Damage.

Ultraviolet radiation is efficiently absorbed by most organic substances, which causes many photochemical reactions in the living cells. The nucleus of each cell consists primarily of genetic material in the form of DNA.

Technetium (99m Tc) sestamibi (commonly sestamibi; USP: technetium Tc 99m sestamibi; trade name Cardiolite) is a pharmaceutical agent used in nuclear medicine drug is a coordination complex consisting of the radioisotope technetiumm bound to six (sesta=6) methoxyisobutylisonitrile (MIBI) anion is not defined.

The generic drug became available late September   Based on Cell Cycle []. Cells propagate through division through a series of events.

Radiation resistance through the cell cyle correlates with the level of sulfhydryls which are natural radiation are most sensitive in the M phase and often G2. Slow cycling cells are resistant in early G1 and sensitive in late G1.Sigma-Aldrich offers abstracts and full-text articles by [Nukhet Aykin-Burns, Benjamin G Slane, Annie T Y Liu, Kjerstin M Owens, Malinda S O'Malley, Brian J Smith, Frederick E Domann, Douglas R Spitz].