05. Radiation Toxicity
Radiation Oncology Radiation oncologists duties firmly with medical oncologists, surgeons and other doctors to coordinate the most suitable care for you. Radiation therapy uses targeted and regulated doses of high-energy radiation to destroy cancer cells.I delighted to share my knowledge as field specialist with this blog.
Cellular Response for Ionizing Radiation
Radiation sources are all around the environment and every
time we are exposed to different kinds of radiation from low-frequency to high-frequency electromagnetic range. Studies of radiation mainly use for radiotherapy
and space exploration. Biologically cells respond to radiation depending on
their energy. When we consider radiotherapy it exposed cells intentionally
and damages cell structures which cell harmful to the body with various mutations
called tumors. Progress of this treatment depends on the radioresistance of tumor
cells and induced damage to normal cells located near to tumor.
Increasing radiodensities of tumor cells and specific radioprotection of normal
tissues are strategies used to decrease the amount of damage to normal cells in
radiotherapy, in a Space environment definitely produce highly protective fabrics
and covers to reduce endanger of astronauts from cosmic radiation.
As mentioned in my previous blog qualities of ionizing
radiation depend on mean energy deposition per track length called Linear
energy transfer (LET). (Radiation
Sources in Cosmic Environment). Ionizing radiation is caused mainly for DNA
damage or changes in sequence. DNA and ionizing radiation interact in two ways: direct action and indirect action.in Direct action initiate
with high LETs hit the DNA and caused double-strand breaks and producing lethal damage.in
indirect action, ionizing radiation is induced for the ionization of water molecules
and produces OH- radicals (H2O→ H+ + OH-)
and damage DNA by its electrostatic changes.
When DNA damage from ionizing radiation double strand breaks is mostly lethal.in beginning, the DNA damage response (DDR) initiates the arrest cell cycle and facilitates DNA repair and maintenance of the genome. tumor suppressor protein p53 is then activated by various phosphorylating kinases responding to release within DNA damage and arrest cell cycle from G2 to M phase. Repairing DNA will initiate nonhomogeneous end joining (NHEJ) or homogenous recombination (HR). NHEJ can repair DSBs throughout the cell cycle but during the G1 phase. But it will become inaccurate and complete DNA with error because its repair process depends only on correcting complementary overhangs and just phosphorylate 5’ and 3’ ends. In contrast, HR is less free cause it requires an error-free sister chromatid for recombination but the issue is HR is only available in the late S or G2 phases. If the repairing process is completed successfully, the cell will continue its cell cycle and undergo repopulation but DNA improper repair initiate cell death by apoptosis, mitotic death,or senescence.
Stay Tuned!
LinkedIn: linkedin.com/in/sachindra-lochana-603131202
Comments
Post a Comment