Radiation and radioactive materials

Question 1

Ionizing radiation

Answer 1

Radiation that has sufficient E to displace electrons from molecules
Sources: radon gas, background radiation, atomic weapon, nuclear accidents, medical treatments

There are two types:
Particular: alpha, beta, proton, neutrons
Need to be ingested/inhaled to cause damage=poor penetrating power
Beta have more penetrating power than alpha
Particle collision decrease penetration and charge repulsion in air(dont travel far)
Electromagnetic waves: x-ray, gamma ray
Penetrate deep into tissue, zero mass and uncharged so tend to scatter and deflect easily = deeper penetrati

Question 2

Radionuclides

Answer 2

Radioactive atoms that release both electromagnetic and particle radiation as they decay. Unique to each type of radionuclide
Directly ionizing bc they collide with electrons of atoms
Indirect ionization via photon transfer E to electron

Question 3

Units of activity

Answer 3

Becquerel: 1Bq = 1n= nuclear disintegration/second
Dose: basic unit of dose is gray(Gy)=amount of E released per mass of tissue
1 Gy = 1J/kg tissue

Question 4

Linear energy transfer(LET)

Answer 4

Rate of dissipation of E from a single event, how much E particle gives off as it travels thru tissue.
Average E loss due to interaction per unit length of its trajectory
Units are kiloelectron volts per micrometer(keV/microm)
X-ray, gamma-ray and Beta particles produce limited ionization tracks = classified as low LET radiation
Particulate radiation-neutrons and alpha particles- tend to have more collision and dissipate more E = HIGH LET

HIGH LET CAUSES MORE DAMAGE THROUGH DS DNA WHILE LOW-LET NO OR SS DNA DAMAGE.

Question 5

Absorbed dose->equivalent dose(Ht)->effective dose(E)

Answer 5

Dose and damage:
biological damage caused by a certain dose of radiation varies based on type of radiation.
LET is important
Relative biological effectiveness(RBE): come from concept of these differences and approaches used to understand equiv dose

Question 6

Equivalent dose(Ht)

Answer 6

Ht = Wr X Dtr Units in Sieverts (Sv – the dose in Gy multiplied by a quality factor)      Dtr = Dose of radiation of type R to the organ(Gy)
Wr= Radiation weighting factor (different for different radiation, reflects LET value-relative to damage they cause)=radiation higher damage=hi number

Question 7

Effective doses(E)

Answer 7

Different tissue have differential sensitivity to radiation
Equation E(Sv)= WtHt
Ht = equivalent doses
Wt= summation of tissue multiplied by Wt

One SV effective dose = 4% change of fatal cancer, 0.8% hereditary defect in kid

Question 8

Mechanism of DNA damage

Answer 8

Ionizing radiation slow down when it forms ion pairs(positively charged atom and an electron)
Leave a track of damage
Low-LET radiation(X-/gamma-rays)= produce a few ionizaitons across an average cell nucleus
More likely to produce isolated damage that CAN be repaired by enzymes
SS dna break, damage bp, LOW DS BREAKS, less crosslinks
More breaks but they’re “simple” and ez repair
High-LET alpha particle= produce thousands of ionization to a cell
Produce clustering of damage that can severely disrupt DNA and make it difficult or impossible to repair
Fewer lesions but “complex” breaks including DS, SS, damage to base pairs all in close proximity-harder and irreversible repair

Question 9

DNA damage response(DDR)

Answer 9

DDR following radiation exposure occurs via 3 types of protein
Sensors: amplify the damage signal via transducer proteins and senses DNA breaks-Can track to measure damage-gammaH2AX Ab
Transducer: signals damage downstream effector proteins
Activator: Effector proteins can lead to cell cycle arrest, apop or repair

Question 10

Tracking damage-sensor proteins

Answer 10

GammaH2AX Ab: sensor protein for DS DNA breaks
GENOMIC INSTABILITY: increase rate of acquiring genetic change. This increases malignancy risk, persisting for many generations, chromosomal translocations.
May be a result of decrease in telomere repair mechanism or loss of the telomeres due to DS breaks
Uncapped chromosomes more likely to undergo rearrangements

Question 11

Adaptive response

Answer 11

Some cells appear more resistant to radiation damage if they are exposed to a low “priming dose” of radiation.
ADAPTIVE RESPONSE(hormesis): initial low dose up-regulates DNA-repair pathways, are then able to better deal with subsequent large insults

Question 12

Models of risks

Answer 12

LNT-linear non-threshold: no matter the dose, exposure increase risks
Hypersensitivity: low dose we are hypersensitive/damage
Threshold: certain dose exposure = nothing occurs but once inc dose = damage
Hormesis: low levels, cell protect by upregulating repair mech
Epidemiological data: 100mSV lowest dose we associated with cancer in humans(cant extrapolate below this dose)

Question 13

Case study: Chernobyl

Answer 13

Power plant meltdown releasing isotopes Iodine(131), Cesium(134), Cesium(137)
Ingestion of Iodine(131) allow it to reach thyroid gland = thyroid cancer
Government treat by stocks of iodine pills so that stable iodine will outcompete radioactive version for uptake into gland

Question 14

Acute radiation sickness(ARS)

Answer 14

Massive whole-body irradiation of 1grey or more induce ARS
Consist of 4 stages(PLIR):
Prodromal stage: nausea and/or vomiting(GIT issue w/ blood)
Latent stage: patient appears recuperate
Illness stage: 3-5weeks=CNS disorder(seizure, ataxia, loss of motor control), CV shock, pulmonary edema, hematological changes, cutaneous syndrome
Recovery if survive

Question 15

Radiation Treatment

Answer 15

DTPA: zinc or calcium diethylenetriaminepentaacete- CHELATOR for internal radiation, doesn’t help DNA damage
Exchange its calcium or zinc for radionuclides
Results in increase urinary excretion of radionuclides