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toxicology > Carcinogens > Flashcards

Carcinogens Flashcards

1
Q

what percentage of cancers are caused by environmental causes

A

80%

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2
Q

what are the 5 groups of carcinogens

A 
alkylating agents
aromatic amines
azo dyes
nitroso compounds
polycyclic aromatic hydrocarbons
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3
Q

what are the specific types of environmental causes of cancer

A

toxins
UV/ionising radiation
oncogenic viruses
man-made carcinogens

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4
Q

how many forms of PAHs are produced and how

A

700 by conbustion of hydrocarbons

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5
Q

how are we exposed to pahs

A

diet, inhilation, lipophilic absorption through skin

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6
Q

why do pahs bioaccumulate but not biomagnify

A

due to enzymatic detoxification

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7
Q

why is persistence of pahs limited

A

photodegradation

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8
Q

what was the first pah to be discovered

A

3,4-benzopyrene

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9
Q

what is the structural simalarity between the most potent chemicals

A

phenanthrene nucleus

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10
Q

what is the K region of the phenanthrene ring

A

the area of highest electron density

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11
Q

what property of the K ring allows interaction with DNA

A

planar

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12
Q

what name is 3,4-benzopyrene also known by

A

benzo-a-pyrene

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13
Q

what did pullmans electronic theory (1950) show

A

link between K region and carcinogenicity

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14
Q

what was thought to be important in carcinogenicity and what was proven otherwise

A

L:K:M balance of electron densities

found its actually the active metabolites which are carcinogenic

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15
Q

who first observed that the metabolites were in fact the carcinogens by putting benzopyrene but not the parent compounds on mice skin

A

elizabeth miller (1950s)

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16
Q

who linked DNA binding to carcinogenicity and in which decade

A

Brooks and Lawley 1960s

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17
Q

which cytochromes produce 7,8-epoxides of the K region

A

chytochromes p450 1A1 1A2 1B1

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18
Q

what are the three methods of epoxide degradation

A

hydrolases convert it to a trans7,8- diol
glutathione peptide conjucation
spontaneous isomerisation to phenols

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19
Q

what percentage of k region epoxides are left after to bind to DNA

A

5%

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20
Q

are diol products more or less toxic

A

more

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21
Q

which trans-diol epoxide was found to bind DNA to a greater extent than 3,4-benzpyrene

A

7,8-dihydrodiol

22
Q

what percentage of epoxides form above the ring (+ enantomer)

A

98%

23
Q

what is Cyt p450 also known as

A

CYPs

24
Q

what is the 7,8-diol produced by the mitochondiral epoxide hydrolase next converted to

A

7,8-diol-9,10-epoxide

25
Q

which form + or - is the diol in

A

-

26
Q

which enatomer is thought to be the ultimate carcinogen

A

the (+) 7,8-diol-9,10-epoxide

27
Q

whih residue to the diol epoxides mainly bind

A

guanine

28
Q

why will the epoxide ring open to form an electrophilic carbinium ion at C10

A

the ring is strained

29
Q

which atom does the epoxide bind

A

NH2 amine or N7

30
Q

what 4 step do pahs increase their metabolism

A

bind aryl hydrocarbon receptor in cytoplasm
transported to nucleus using chaperones
binds ARNuclear transporter heterodimer to bind to gene promoters
increases synthesis of CYPs 1A1 1A2 1B1

31
Q

how does PAH binding cause carcinogenicity

A

causes damage to dna, repair not always acurate

32
Q

what are the critical genes in which mutations occur

A

proto onco genes (ras) and tumour supressor genes (p53)

33
Q

what percentage of tumours are caused by ras mutations

A

10

34
Q

which group of proteins do ras genes encode

A

p21

35
Q

what has been lost from oncogenic p21 and what is the resut

A

GTPase activity

constantly activated

36
Q

what is the role of p53

A

accumulates around damaged dna to allow repair to occur

induces apoptosis if repair fails

37
Q

what effect does muttion often have on p53

A

inactivation

38
Q

what can affect susceptibility to chemical carcinogens

A

expression of enzymes involved in metabolism of carcinogens
mutations in enzymes involved in metabolism
efficiency of dna repair

39
Q

what is usually the target organ of PAHs

A

liver

40
Q

what can be used as biomarkers of pah exposure

A

binding of electrophilic metabolites to proteins and dna

41
Q

what can be used to assay pah exposure

A

haemoglobin and albumin

42
Q

what are the effects of pahs aside from cancer

A

phototoxicity
cardiovascular disease (atherosclerosis)
foetal malformations
disruption of development 3-6 years

43
Q

what are the adverse affects which arent cancer caused by

A

activation of aryl-carbon receptor

44
Q

how is damage to DNA detected

A

distortion of helix

45
Q

what isthe general process of dna repair

A

xp proteins provide scaffold, helicase unwinds dna, incisions by exonucleases remoce 27-29bp, dna polymerase delta and epsalon extends dna with high fidelity, dna ligase joins bases together

46
Q

under what circumstances are mismatches in dna not recognised and why

A

durin cell replication

uses low fidelity polymerase

47
Q

what is the common mutation caused by 3,4benzopyryne damage

A

g to t

48
Q

what is the common mutation caused by uv damage

A

c to t

49
Q

what are the 6 hallmarks of cancer

A 
apoptosis evasion
increased growth signals
insensitivity to anti growth signals
unlimited replication potential
sustained angiogenesis
tissue invasion and metastasis
50
Q

why are most cancers found in eptithelial cells

A

most exposure and most repair and mutations

toxicology (11 decks)

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