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Biophysics > 41-53 > Flashcards

41-53 Flashcards

Free radicals

1
Q

free radical

A

species that contains 1 or more unpaired electrons

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2
Q

EG of radicals

A 
O2-. superoxide anion radical
O2.-2 peroxide radical
.OH Hydroxyl radical
No. Nitric oxide radical
RO2. Peroxyl radical
1O2 singlet oxygen
H. Hydrogen radical
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3
Q

when 2 FR meet

A

unpaired electrons join to form pair and both radicals are lost

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4
Q

oxidative stress

A

when FR generations exceeds capacity of AO defenses

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5
Q

diseases associated with superoxide anion radicals

A

O2-.
inflammatory disease=glomerulonephritis= inflammation of glomeruli of kidneys

radiation induced cancer

strokes

wilson’s disease= Accumulation of Cu

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6
Q

source of FR generation in body

A

Endothelial cell lining blood vessel respond to certain stimuli (EG ACH (Para-Sym NS) or bradykinin) by secreting Nitric Oxide radical = relaxes smooth muscle = vasodilation = decreases blood pressure

When water exposed to IR = H20–> H. radical + .OH
Hydroxyl radical more dangerous than nitric oxide radical as it is extremely reactive

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7
Q

why is hydroxyl radical so dangerous

A

extremely reactive, attacks to all molecules in cells, it fragments DNA(carcinogensis)/proteins/carbohydrates
initiates lipid peroxidation
will start a FR chain reaction to degrade tissue

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8
Q

SOR formed by

A

O2-. adding 1 electron to Oxygen

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9
Q

is SOR more or less reactive to hydroxyl radical

A

O2-. < .OH

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10
Q

what happens when SOR reacts to NO.

A

opposes vasodilator action of nitric oxide radical = acts as vasoconstrictor

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11
Q

is SOR good or bad

A

O2-. can be useful
acts as growth regulators due to continuous generation in small amounts by lymphocytes and fibroblasts

useful in phagocytosis when NADPH-Dependent superoxide synthase/enzyme activate to produce large quantities of 02-. to kill invading pathogens

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12
Q

how is singlet oxygen 1O2 formed

A

when photosensitizing agents react w/ ground state oxygen O2

1^S + hf ->3^S*
3^S*+3^O2->1^S + 1^O2

1^S = ground singlet state
hf = photosensitizing agent
3^S*=oxidised photosensitiser FR
1^O2=singlet Oxygen

EG photosensitizing agent=porphyrin
Accumulation of porphyrin will damage skin to form singlet oxygen
==this can be useful since hematoporphyrin is taken up by cells, so by using fluorescents we can identify sites of tumor

Peroxyl radicals will collide w/ each other to form small amounts of singlet O2

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13
Q

how is hydrogen peroxide formed and is this dangerous

A

oxidation of certain AA in peroxisomes, yes since when H2O2 reacts w/ superoxide anion radical = hydroxyl radical

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14
Q

why are cell membranes prone to FR attack

A

free poly unsat FA on cell membranes are readily attacked and oxidize into lipid peroxides = damages body cells and releases toxic products

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15
Q

initiation and propagation of lipids

A 
I=RH+X.->R.+XH
RH=unsat lipid
X.=Radical
R.=Lipid radical
XH=EG. Water 
P= R.+O2->ROO.
ROO.+RH->ROOH+R.
ROO.= peroxyl radical
ROOH=lipid peroxide
R.=lipid radical
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16
Q

what can Peroxyl radicals do

A

abstract H atoms from adjacent PUFA side chains to propagate FR chain reaction of lipid peroxidation

reacts w/ AA residues on proteins = impairs function

oxidizes cholesterol = products will promote atherosclerosis

2 RO2. react with each other:
2RO2. ->R2O4->R2O2 + 1O2 singlet oxygen

17
Q

decomposition and termination of lipid peroxidation

A

D:
H2O2/ROOH+Fe2+-complex->Fe3+-complex+-OH+.OH/.OR

ROOH+Fe3+-complex->Fe2+-complex + H+ + ROO-

HOOH=hydrogen peroxde
ROOH=lipid hydroperoxide
Fe2+-complex=ferrous ion complex
Fe3+ complex= ferric ion complex
-OH=hydroxide ion
.OH=hydroxyl radical
ROO-=Peroxyl ion
.RO=alkoxy radical

T=R.R.->RR
R.+RO2.->R2O2
ROO.+ROO.->R2O4

R.=C centered radical
RO2.=Lipid peroxyl radical

18
Q

consequences of lipid peroxidation

A

increased membrane rigidity, decreased activity of membrane bound enzymes EG Na+ pumps, altered activity of membrane receptors and altered permeability and function of membrane

19
Q

enzymatic AO EGs

A

Superoxide dismutase SOD, Catalase and Glutathione Peroxidase

Fe bound to transferrin and Cu bound to ceruloplasmin to prevent lipid peroxidation

20
Q

Superoxide dismutase function

A

Superoxide dismutase in mitochondria and cytosol.

catalyses removal of superoxide anion by 10000 fold
2O2-. + SOD -> O2+H2O2

in peroxisomes, AA oxidases involved

21
Q

catalase function

A

found in peroxisomes in E

degrades H2O2-> water and oxygen 3O2/triplet oxygen

it finishes the detoxification reaction started by Superoxide dismutase

22
Q

Glutathione peroxidase reaction and function

A

Glutathione peroxidase = G-Px - group of enzymes that degrade hydrogen peroxide and PUFA peroxides to metabolize released peroxides

23
Q

Non-enzymatic AOs EGs

A

Alpha-Tocopherol/ Vitamin E and Vit C

24
Q

Alpha-Tocopherol/Vit E function

A

Alpha-tocopherol/Vit E is a lipid-soluble AO and reacts to peroxyl radicals faster than peroxyl radicals and PUFAs.

It reacts w/ the RO2./Peroxyl radicals to migrate to membrane surface to be reduced back to alpha tocopherol in reaction w/ Vit C/ascorbic acid to minimize rate of Lipid peroxidation

25
Q

Ascorbic Acid/Vit C function

A

helps in function of alpha-tocopherol/vit E to minimize rate of lipid peroxidation

26
Q

what does oxidative stress lead to

A

atherosclerosis = narrowing of arterial lumen = myocardial and cerebral infarcts(tissue death due to inadequate blood supply) = tissue ischemia

also oxidative stress leads to CNS injury=stroke

27
Q

how is atherosclerosis caused

A

due to the impaired endothelium, monocytes adhere here and develop into macrophages to produce superoxides

also lipid-laden foam cells found in the early lesions will undergo peroxidation here

28
Q

which places in the human body are more prone to oxidative stress and why

A

brain and spinal cord

their membranes are rich in PUFA side chains but the AO activity is low. So any injury can release intracellular ions that accelerate FR reactions and peroxidation of brain lipids.

Also NS is rich in epinephrine, norepinephrine, dopamine, these hormones can react with oxygen and form superoxide radicals that participate in FR reactions

29
Q

what is used to reduce damage caused by oxidative stress in brain and spinal cord

A

chelating agents can bind to Iron to inhibit peroxidation of brain homogenates and prevent it accelerating FR reactions. But these complexes must cross the brain-blood barrier.

30
Q

what makes AO efficient

A

must protect proteins/DNA from oxidative damage

their method of protection must be to scavenge radicals, prevent radical formation, repair the damage done by radicals

Biophysics (4 decks)

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