The less mature cells are more radiosensitive than the more mature cells So cell in active mitosis like the stem cells are more affected than cells that divide slowly like neurons

2.  The less mature cells are more radiosensitive than the
more mature cells
 So cell in active mitosis like the stem cells are more
affected than cells that divide slowly like neurons

3.  However later experiments on flies have shown the
ionizing radiation is capable of mutation induction
which can be similar to some extent to spontaneous
mutation in nature
 The effects of these radiation depends on the total
dose and the duration of exposure

4.  Injury following radiation exposure may be not
specific as can occur due to chemical or heat exposure
 There is a period of latency for observable response to
happen that may range from decades for low radiation
doses to minutes of hours for larger doses

5. Direct
interaction
Indirect
interaction

6.  The cell’s macromolecules as proteins and DNA are hit
by ionizing radiation and they are either killed or
mutated
 It is hard to permanently destroy or break double
stranded DNA than single stranded DNA
 However certain cells react as if they contain single
stranded DNA so being more radiosensitive

7.  It the hit causes complete break or permanent damage
of DNA these cells die or eventually die
 However humans have abundance of cellular repair
process that can replace the died ones
 Only when this replacement mechanism falters , the
radiation effects are seen which occurs probably at
higher doses of radiation

8.  Actively dividing cells are more sensitive
 Among the 4 stages of cell division the M phase when
the chromosomes are condensed and paired is the
most radiosensitive
 Cancer cells being more dividing and having more
chromatin in them are considered more radiosensitive
than the normal cells

9.  This occurs when the radiation injury is deposited in
the cells
 The interaction here occurs with the cellular water not
with the macromolecules
 Hydrolysis of water ultimately results in the formation
of hydrogen peroxide which further affects many
cellular processes inside the cells
 Here comes the role of antioxidants as anticancer
agents

11. Division delay
Reproductive
failure
Interphase
death

12.  Dose dependent pattern with doses from 0.5 Gray to 3
Gy
 After a period of delay it returns back to near normal
for unknown reasons
 However above the dose of 3 Gy the mitotic rate may
not recover the division may never happen

13.  It is also dose dependent
 At doses below 1.5 Gy it occurs in random non linear
pattern
 However above 1.5 Gy it is non random and linear

14.  Cell death can occur many generations from the initial
radiation exposure
 It is thought it can be due to apoptosis or arrest of cell
replication
 Immature rapidly dividing cells are more sensitive

15. As a general role,
any type of cell
injury as a result of
direct or indirect
interaction with
ionizing radiation

16. Linear threshold
Linear no threshold
Linear quadratic

18. Stochastic
Non
stochastic

21. Acute effects
Chronic effects

22.  Ionizing radiation are considered harmless at the
diagnostic or background level
 Above the dose of 0.5 Gy effects start at a linear fashion
and in non stochastic pattern
 Some chromosome aberrations may be seen at doses
below 0.5 Gy but with no clinical symptoms

26.  They are primarily stochastic
 Cancer is the primary concern
 However non cancerous effects like cataract may also
occur
 Leukemia may occur as one of stochastic effects of
radiation with doses of 50-100 rads
 At doses of 100-500 rads there is a linear relation with
leukemia

27.  Data suggest that the rate of leukemia incidence by 1-2
cases per million with every rad of exposure
 There is a latency of 14 years
 Higher doses are associated with other types of cancer
like lung, bone, thyroid etc

29.  Depletion of BM and peripheral blood cells together
with loss of lymphoid organs weight are well
established side effects
 MSCs seem more radioresistant than the HPSCs
 This may be attributed to oxidative stress resistance

30.  This observation was confirmed with the finding in
transplanted patients received TBI showing the MSCs
are the host’s not the donor’s indicating radio-
resistance
 MSCs also retain their differentiation ability shown by
the increased adipocytes in BM of murine models
achieving bone marrow failure

31.  This preferential differentiation towards adipocytes
comes at the expense of osteoblasts explaining
osteoporosis and altered bone marrow
micorenvironment following irradiation exposure