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Rad Bio > Exam 1 > Flashcards

Exam 1 Flashcards

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Biology 101 flashcards
1
Q

calculation of Dq

A

quasi threshold dose
a large Dq can more easily cover than a cell with low Dq
the dose at which the straight portion of the cell survival curve extrapolated backward cut the dose axis drawn through a surviving fraction of one

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2
Q

If Do= D1

A

n will equal 0

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3
Q

variations in radiation sensitivities

A

low let RT shows a wide range of sensitivity these differences are reduced when it comes to Hi-Let radiation. This difference is due to the size of the shoulder

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4
Q

Intrinsic cell radio sensitivity

A

increasing Do indicates more resistant cells

cells from tumors have a broad range of radiosensitivities

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5
Q

Cell classifications

A

Vegetative inter-mitotic
differentiating inter mitotic
reverting post mitotic
fixed post mitotic

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6
Q

vegetative inter mitotic

A

produce cells like themselves, go through mitosis regularly

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7
Q

differentiating inter mitotic

A

divide regularly, some differentiation

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8
Q

reverting post mitotic

A

dont divide regularly, but can if needed

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9
Q

fixed post mitotic

A

do not divide, highly differentiated

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10
Q

plating efficiency (PE)

A

percentage of untreated seeded cells that grow into a colony

PE= (number of colonies)/(number of cells plated) x 100

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11
Q

Survival fraction (SF)

A

Fraction of cells surviving a given dose is determined by counting macroscopic colonies and allowing for plating efficiency
SF = (colonies survived from radiation)/ (total cells initially seeded x (PE/100))

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12
Q

High LET cell survival curves

A

Straight on semi-log plot

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13
Q

Low LET cell survival curves

A

have slope, shoulder and subsequent straight region

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14
Q

Linear quadratic relationship

A

S= e^(aD+bD^2)
a= initial slope
b= quadratic component
ratio of a/b is dose at which linear and quadratic components are equal

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15
Q

Cell mitotic death

A

majority of tumor cells have mitotic death as dominant feature, thus follows linear-guadratic model

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16
Q

Apoptic death

A

if apoptosis dominates, cells are radiosensitive if absence radio resistant

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17
Q

Cell death

A

for cells in G0 it is the loss of function

for cells in M it is the loss of capacity to divide

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18
Q

in context of radiobiology

A

if a cell losses its capacity to divide indefinitely and cant produce a colony it is considered dead

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19
Q

types of cell deaths

A

apoptosis
mitotic death
autophagy
senescence

cause cell to lose ability to proliferate indefinitely

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20
Q

apoptotic death (programmed cell death

A

radiosensitive
lymphoid cells
majority of cells NO apoptosis upon radiation

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21
Q

Mitotic death (passive)

A

most common form of cell death from radiation exposure

death due to damaged chromosomes

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22
Q

how to measure RT induced cell death

A
  1. In Vitro
  2. In Vivo (in situ)
  3. in Vivo ( ex situ or ex vivo)
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23
Q

In Vitro

A

COLOGENIC ASSAY

trypan blue exclusion assay

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24
Q

In Vivo (In Situ)

A

skin (pig skin) intestinal crypt cells, testes kidney tubules

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25
Q

In Vivo (ex situ or ex vivo)

A

SPLEEN COLONY ASSAY

tumor transplant

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26
Q

Cologenic Assay

A 
tissue culture techniques-
specimen taken from organism
chopped into small pieces
single cell suspension prepared by use of enzyme trypsin
cell plated onto culture dish
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27
Q

Increasing LET survival curves

A

increases slope of survival curve
results in more linear curve
shoulder disappears due to increase of killing by single events

28
Q

Relevant doses

A

100gy - destroys cell function in non-proliferating systems (nerve, muscle cells)
2gy mean lethal dose for loss of proliferative capacity (blood)

29
Q

features of survival curve

A

low doses -shoulder
intermediate doses- region where survival curve bends and survival shows greater change with increasing dose
high dose- region where survival falls rapidly with dose

30
Q

general survival models

A

multi target model- based on hitting the target
linear-quadratic model- dual radiation actions
1- cell killing is proportional to dose
2. cell killing is proportional to square of dose

31
Q

factors regulate therapeutic ratio

A
  1. TUMOR SIZE
  2. DOSE RATE EFFECT
  3. TIME INTERVAL
  4. LET of radiation
  5. PResence of radio-sentizers/ protectors
  6. Plan design and precision of implementation
32
Q

cell cycle resistant stages

A

S phase most resistant

G2 and M most sensitive

33
Q

4 r’s

A
  1. REPAIR
  2. REDISTRIBUTION
  3. REPOPULATION
  4. REOXYGENATION
  5. radiosensitivity
34
Q

operational classification of radiation damage

A
  1. lethal damage
  2. potentially lethal damage
  3. sublethal damage
35
Q

lethal damage

A

irreversible, irreparable

36
Q

potentially lethal damage

A

modified by post irradiation environment conditions

37
Q

sublethal damage

A

can be repaired under normal circumstances

38
Q

types of dna damage

A 
abasic site
base damage
bulky base damage
single strand break
double strand break
interstrand cross-link
39
Q

types of simple repair

A

chemical repair
direct reversal of damage
1. photolyase- revert UV induced pyrimidine dimers by using visible light
2. methyl transferase- removes methyl group from damage base and adds it to itself

40
Q

excision repair

A

base excision repair
nucleotide excision repair
mismatch repair

41
Q

base excision repair

A

DNA glycosylase cuts out damage base- dna polymearse fills the gap. (single nucleotide cut out)

42
Q

nucleotide excision repair

A

large strand removed and replaced

43
Q

mismatch repair

A

proofreading of replication endunuclease makes a cut in the newly synthsized strand

44
Q

Repair of DNA strand breaks

A

A. DNA single strand break repair

B. DNA double strand break repair

45
Q

DNA single strand repair

A

exonuclease extends the gap- DNA poylmerase fills in the gap- dna ligase seals the strands- part of the base excision repair machinery

46
Q

DNA double strand break repair

A
  1. non-homologous end joining- error prone

2. homologous recombination repair - error free

47
Q

Lack of DNA repair

A

mutagenesis
chromosome aberrations
microsatellite
cell death

48
Q

mutagenesis

A

if DNA damage not repaired before S-phase - DNA polymerase may put in wrong base mutations: silent, frameshift, deletions

49
Q

chromosome aberrations

A

IR; errors in repair most chemicals: complications during replication of damaged template

50
Q

microsatellite instability

A

loss of mismatch repair- slippage errors during replication

51
Q

cell death

A 
if cell is not able to resolve blocked transcription or blocked replication cell death- premature aging
apoptosis
autophagy
necrosis
mitotic catastrophy
52
Q

carcinogenesis

A

initiation-> promotion-> transformation-> progression

53
Q

genes involved in carcinogenesis

A

proto-oncogenes-> oncogenes
tumor suppressor genes (gatekeepers)(p53,Rb)
DNA stability genes(caretakers)

54
Q

autophagy

A

genetically controlled, formation of double membrane casuoles in cytoplasm sequestering mitochondria and ribosomes

55
Q

apoptosis

A

suicide, genetically controlled, executed by caspases and nucleases, cell shrinkage, dna degradation

56
Q

necrosis

A

‘murder’ passively occurring, cell swelling

57
Q

mitotic castastrophy

A

caused by mis-segregation of chromosomes, often form “micronuclei’, ‘giant’ cells or multinucleate cells, could induce apoptosis

58
Q

spurs

A

<100eV

59
Q

blob

A

100-500eV

60
Q

short track

A

<5000eV

61
Q

branch track

A

> 5000eV

62
Q

direct action of radiation

A

radiation absorbed directly by the target

63
Q

indirect action of radiation

A

radiation energy absorb in non-target molecule that then becomes reactive and attacks the target

64
Q

the hydroxyl radical

A 
one unpaired electron
uncharged
very reactive
can damage dna if formed close to dna molecule
major contributor to indirect IR
65
Q

radical scavengers

A

give up electorns to radicals

can also donate hydrogens to radicals leading to chemical repair

Rad Bio (1 decks)

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