Oxidative Balance Flashcards

1
Q

ROS

A

reactive oxygen species;

molecular O2, OH-, OH. (radical), superoxide O2-. (1 unpaired and charged)

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2
Q

RNS

A

reactive nitrogen species; nitric oxide NO. (1 unpaired)

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3
Q

unstable O-O bonds

A

H2O2 bonds, ONOO-

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4
Q

cell to cell messages via NO

A

smooth muscle relaxation, vasodilator, neurotrans, hair follicle life cycle;
endothelial cells with NOS release NO and they react with guanylyl cyclase in smooth cells–> vasodilation

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5
Q

NO synthase

A

L-arginine undergoes reaction with NOS (1,2,or 3) and turns into L-CItrulline + NO.
Uses 2 NADPH

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6
Q

What inhibits NO

A

Myoglobin

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7
Q

Intracellular ROS

A

superoxide (made through leaky electrons in the ETC pathway); superoxide dismutase binds the superoxide and binds free radical and makes hydrogen peroxide

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8
Q

hypothesis of superoxide

A

metabolic state of the cell determines superoxide activity; more ETC activity–> more superoxide; the receptor proteins sense change and the transcriptome/proteome responds

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9
Q

e- in the process of O2 causes

A

free radicals

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10
Q

enhancing ROS production during ETC

A

high ETC–> make more ADP, slow down TCA (ADP limiting factor)

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11
Q

diminish ROS production during ETC

A

uncoupling protein transports H+ into inner membrane without making ATP and ETC is low. Adapt needed–> increase CA cycle;

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12
Q

ROS in inflammation and immunity

A

NADPH oxidase and arachidonic acid catabolism

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13
Q

NADPH oxidase

A

in neutorphils;
NADPH redox reaction to NADP which removes e- and reacts with O2 to make superoxide going into phagocytic vesicle or go outside cell;
it’s the first line of defense against infection

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14
Q

how is superoxide used against bacteria?

A

bacteria are rich in unsequestered Fe2+. Superoxide with protons creates H2O2 which then reacts with Fe2+ via fenton reaction to create more HO. + OH-+ Fe3+

free radicals and metals–> snowball affect

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15
Q

arachidonic acid catabolism

A

signaling: inflammation and immunity
messengers: nervous system
direct result of autooxidation;
creates leukotrienes and prostanoid eicosanoids

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16
Q

haber-weiss reaction

A

superoxide and hydrogen peroxide make more hydroxy radical and hydroxy anion and O2 via free iron

17
Q

ROS attack

A

bases and backbone of nucleic acids, amino acid side chains, double bonds of unsaturated fatty acids;
non specific

18
Q

dityrosine bridges

A

cross linked protein which cannot be degraded via proteosome; created via cysteine, lysine, proline, arginine, metionine cross links

19
Q

oxidative damage: membrane

A

via arachidonic acid it creates peroxy cpds, hydroperoxy cpds, OH radical and isoprostanes which lead to rancid membranes

20
Q

PUFA chain reaction

A

depletes membrane unsaturated fatty acids; diminished fluidity of membrane

21
Q

oxidative damage to macromolecules

A

DNA mutagenesis, protein loss of function, protein aggregation, impaired protein disposal, loss of membrane fluidity, toxic lipid peroxidation byproducts

22
Q

generalized control of ROS

A

redundant, enzymatic, nonenzymatic

23
Q

superoxide dismutase

A

acts on superoxide

24
Q

catalse

A

acts on hydrogen peroxide

25
Q

glutathione peroxidase/reducase

A

acts on H2O2;

inactivated by nonspecific glycation in diabetes

26
Q

thioredoxin enzymes

A

peroxiredoxin/thioredoxin reductase, variety of substrates

27
Q

SOD

A

superoxide dismutase;

takes two superoxides and combines in to hydrogen peroxide

28
Q

catalase reaction

A

two hydrogen peroxides to two water and one o2 molecules

29
Q

non enzymatic antioxidants

A

tend to be reduced at baseline; accept or donate electrons; become radicals during the process but they are less reactive than neutralized radical because of resonance

30
Q

drawbacks of antioxidant use

A

kidney or liver malfunction changes antioxidant metabolism; may interfere with normal signaling or immune response (NADPH oxidase),

31
Q

why can vitamin c exacerbate kidney stones?

A

one of the metabolites of vitamin c is oxalate. oxalate is a main component of kidney stones