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Biochem Final Flashcards

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1
Q

mito etc

A

inner mito membrane, coupled to ox phos, pH gradient

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2
Q

bacteria etc

A

no mito, so its in the cell membrane. use coq or vit k, pH gradient

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3
Q

photosynthesis

A

driven by light energy, convert co2 to hexose sugars

- located in chloroplast mem

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4
Q

nadph

A

know structure

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5
Q

light reactions

A

photosys 1 generates nadph
photosys 2 splits h2o and forms o2 and reductant
- light required

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6
Q

dark reactions

A

nadph and atp take co2 to make glucose

- no light required

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7
Q

chlorophyll a and b

A

know structure

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8
Q

chlorophyll

A

alternating single adn double bonds make them good photoreceptors
- light is transferred to reaction centers that contain the etc

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9
Q

etc z diagram

A

1) split h20
2) rise in energy and go down etc
3) photosys 1
4) rise to ferodoxin
4) go down etc and back to photosys 1 OR make nadph

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10
Q

microsomal etc

A

found in ER, which does protein synth, transport and has 2 etc

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11
Q

p450 system

A
  • no atp made
  • reox nadph to nadp
  • Oh to groups so you can pee them out in liver
  • need flavorptoein, cyto p450 reductase
  • oh is done by hydroxylase, monooxygenase, mixed function oxidase
  • inductible so can increase if there is a toxin to quickly remove
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12
Q

b5 system

A
  • adds double bonds to fa using nadph
  • can add double bonds to fa but NOT past c9
  • we can’t make linoleic acid (c9,12) or linolenic acid (c9,12,15)
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13
Q

gluconeogenesis

A
  • liver mostly
  • see pathway
  • irreversible is gly to glc 6 p and gructose 6 p to fructose 16 bisp
  • turns to pyruvate
  • made in exercise during lactation or starvation
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14
Q

how pyruvate becomes PEP, biotin problems

A
  • irreversible
  • see process
  • pyruvate carboxylase needs acetyl coa and biotin
  • links to lysine and binds co2 to add it to pyruvate
  • avidin in egg whites stops biotin from binding
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15
Q

pfk reverse step

A

takes fructose 16 to fructose 6

  • fructose 6 phosphate is the enzyme
  • no atp made
  • positive effected by citrate and atp
  • negative by amp
  • ON when atp is present
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16
Q

pfk enzyme

A

positive effectgor is adp and amp

negative is citrate and atp

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17
Q

hexokinase reverse step

A
  • glucose 6 phosphatase that turns it back to glucose
  • found in liver and kidney only
  • liver is primary source of blood glucose
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18
Q

glycogen synthesis

A
  • see diagram
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19
Q

phosphoglucomutase

A

takes glucose 6 p to 16 p

- reversible

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20
Q

utp glucose pyrophosphatase

A

utp glycose + glucose 1 p to make pyrophosphate and udp glucose
- pyrophosphate makes this irriversible

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21
Q

glycogen synthetase

A
  • does udp glucose + glycogen to glycogen + Udp
  • adds glucose units to non reducing ends of glycogen
  • makes the 1,4 link
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22
Q

how glycogen is elongated

A
  • primer is 4 units
  • every 8-10 it branches using branching enzyme with 1,6 bond
  • more places to break
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23
Q

glycogen phosphorylase

A
  • catalyzes glygocen breakdown by attacking 1,4 links
  • stops 4 units from the branch point
  • transferase takes 3 of the 4 sugars and makes them 1,4 bond
  • debranching enzyme cuts off the last 1,6 and releases

**phosphorylase kinase is activated by ca ions during muscle contraction

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24
Q

glycogen synthetase control

A

I form is no p, active
D form is p, inactive
- d form is allosteric and is off but glucose 6 p is positive effector

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25
Q

glycogen phosphorylase regulation

A
  • p is active, no p is inactive
  • phosphorylase b is effected by atp, glucose 6 p negative
  • adp amp turns it on
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26
Q

epinephrine and glycogen

A

MADE IN ADRENAL MEDULLA

  • acts on muscle
  • g protein cascade
  • activates so taht we get energy when scared, make g6p
  • g6p activates the synthetase to make glycogen
  • epinephrine inactivates it
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27
Q

glucagon and glycogen

A

made in pancreas, acts on liver

- g protein cascade

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28
Q

g protein

A

3 subunits then alpha and beta djssociate to activate

  • stimulates adenylate cyclase, then atp to amp
  • camp is then hydrolyzed to amp by hydrolyase (caffeine inhibited)
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29
Q

camp and protein kinase a

A
  • camp stimulates kinase a, adds p to phosphorylase kinase and synthetase kinase to activate glycogen synthetase and phsophorylase kinase
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30
Q

pentose shunt

A

cytoplasm

  • make d ribose for nucleotide synthesis, nadph
  • no atp made
  • starts with g6p, allosteric enzyme g6p dehydrogenase which is negative by nadph
  • see diagram
  • if pentose needed, then ribose is used
  • if nadph is needed, then ribose is converted back
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31
Q

transaldolase

A
  • takes 3c fragment, needs l stereochem, forms a schiff base with lysine,
  • see diagram

aldo = shoes

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32
Q

transketolase

A
  • transfers 2c fragment

- l stereochem, thiamine pyrophosphate is cofactor

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33
Q

starch meta

A 
forms amylose (14) and amylopectin (16)
- saliva, SI, maltase breaks down last bond
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34
Q

cellulose meta

A
  • b 14

- bulk in diet, no breakdown

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35
Q

sucrose

A
  • sucrase breaks down to glucose and fructose
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36
Q

lactose

A
  • galactose and glucose
  • lactase breaks b14 bond
  • bad in infants to be deficient, switch to formula
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37
Q

fructose entering metabolism

A

pfk and hexokinase turn it to aldose

- pfk deficiency means fructose in pee

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38
Q

galactose entering metabolism

A
  • galactose kinase, transferase, epimerase
  • udp galactose and atp needed
  • epimerase needs nad+
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39
Q

udp glucose and feeding

A

can be made into lactose for nursing mothers, modified by lactalbumin

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40
Q

galactosemia

A
  • disease that causes catacts and liver problems
  • tranferase block: galactose and galactose 1 p build up
  • withold milk
  • can still make udp galactose through epimerase reaction
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41
Q

kinase deficienci=y

A
  • only galactose accumulates
  • onyl cataracts
  • galatitol is made, clouds the lens
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42
Q

blood sugar level regulation

A
  • insulin after you eat, targets white muscle and fat
  • take up glucose in tissues
  • glucose level drops then glucagon
  • liver then does g6p to g breakdown
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43
Q

insulin how it works

A

inhibits synthetase kinase so glycogen synthetase stays active (increase glycogen synthesis)

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44
Q

hypoglycemia

A
  • low blood sugar

- overproduction of insulin so too much sugar uptake

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45
Q

hyperglycemia

A
  • glucose in pee, muscles are depleted in glucose, too much thirst and pee, rapid weight loss
  • ketosis from too much fat breakdown
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46
Q

type 1 diabetes

A

0 insulin is bad

- inject insulin

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47
Q

type 2 dia

A
  • less insulin receptors so glcucose stays high

- eat less sugar

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48
Q

glucose 6 phosphatase deficiency

A
  • can’t do g6- to glucose
  • hypoglycemic
  • glucagon released so high glycogen
  • increase in pyruvate and lactate
  • acidosis
  • TEST: give person glucagon and monitor levels
  • treatment: give small meals of carbs
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49
Q

pfk deficincy in muscle

A
  • can’t do fructose 6 p to fructose 16
  • can’t take sugar thru gkycolysis
  • can’t meta glycogen during exercise fast enough
  • test: no increase in lactate after exercise
  • can be given fructose
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50
Q

glycogen phosphorylase deficiency

A
  • hard to break down glycogen
  • can’t do exercise
  • no rise in pyruvate and lactate levels
  • can give glucose
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51
Q

oxidation of fats location

A

mito then cyto

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52
Q

neutral lipid breakdown

A
  • hydrolysis in cyto of adipose
  • regulated by hormones: gluc and epi turn on camp
  • camp turns on protien kinase, adds p to hormonse sensitive lipase
  • also starvation, stress, esercise and growth
  • glycerol is made and oxidised to dhap to enter glycolysis
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53
Q

insulin and fat breakdown

A
  • unsulin inhibits adenylate cyclase so no tg breakdown
54
Q

phospholipid breakdown

A
  • broken by phospholipase

- snake venom destroys it

55
Q

fatty acid breakdown - outer mito membrane

A
  • coa is attached to the fa, hydrolysis of ppi makes it irreversible
56
Q

how does fa get into the inner mito

A

the long fa chain must be transfered to carnitie (transferase)

  • this is inhibited by malonyl coa
  • then the fa is remade inside
57
Q

fatty acid oxidation process

A
  • uses fad to oxidize
  • trans double bond is formed
  • then add h20
  • use nad to oxidize
  • cleave to make acetyl coa
  • if 16c then need 7 turns to get 8 acetyl coa
58
Q

unsaturated fatty acid ox

A
  • will keep oxidizing until u reach the double bond, then add water to make it l configuration and trans
59
Q

diabetes, insulin and fa breakdown

A
  • unsulin can’t stop hsl in dia, so you get lots of acetyl coa, form ketone bodies, acetoacetate
60
Q

what is needed to fa synthesis

A
  • citrate, co2

- done in cytoplasm

61
Q

how to make pyruvate for fa synthesis

A
  • oxaloacetate to malate then malate goes through malate asp a shuttle OR is converted to pyruvate through malic enzyme
62
Q

acetyl coa carboxylase

A
  • malonly coa is made from co2 + acetyl coa
  • this is done by acetyl coa carboxylase (needs biotin)
  • citrate is positive effector
  • it is a tetramer where one unit binds biotin, one does the co2 and biotin rxn, one transfers co2 to acetyl coa and one binds citrate
  • citrate causes polymerization
63
Q

fatty acid synthetase complex

A
  • malonyl coa binds, found in cyto
  • the fa chain is attached to acyl carrier protein with a phosphopantetheine group
  • see card
  • keeps it from diffusing until palmitate is made
64
Q

how much atp to make fa

A
  • 1 atp for each malonyl coa so 7 atp to make a 16c fa

- nadph comes from pentose shunt and malic enzyme

65
Q

fa breakdown vs synthesis 4

A
  • synthesis in cytoplasm, breakdown in mito
  • acp in synthesis, coa carrier in breakdownn
  • malonyl needed for synth
  • d stereo in synthesis, l in oxidation
  • need nadph for synth, nad and fad for breakdown
  • palmitate is end product for synthesis
66
Q

tg and phospholipid synthesis

A
  • dhap to phosphatidyl serine and phosphotidyl choline
67
Q

inositol lipids

A
  • involved in cascade

- makes phospho inositol

68
Q

sphingolipids

A
  • makes sphingomyelin and cerebroside from palmitoyl coa and serine
69
Q

gangliosides

A
  • formed from cerebrosides + sugars
70
Q

lipid storage disease

A
  • overproduction of lipds (overactive enzymes)

- defected degrading enzymes

71
Q

tay sachs

A
  • defect in enzyme
  • increase in ganglioside gm2
  • can’t do cleavage of n acetyl galactosamine
72
Q

niemann pick

A
  • increase in sphingomyelin because u can’t break it to ceramide and phosphocholine
73
Q

prostaglandin description

A
  • not true hormone since they act on tissue they are made in

- synthesis from linoleic acid to arachidonic acid by cyto b5

74
Q

pge and pgf

A

made from eicosatrienoc acid (pge1 and pgf1)

arachidonic acid makes the 2a

75
Q

prostaglandin synthetase complex

A
  • called cox

turns the arachidonic to pgh2, pge2, pgf2, thromboxne a2 and prostacyclin (pgi2) and endoperoxide

76
Q

biological effects of prostagalndin

A
  • increase camp levels in cell types
  • inflammatory reaction
  • fever
  • muscle contraction
  • platelet aggregation
  • aspirin stops inflammation
77
Q

blood clot mech

A
  • cut, endo is exposed, platelets bind, prostaglandins inhibit this, thromboxanes allow
  • zymogen so not active until cut
78
Q

cholesterol synthesis

A

2 acetyl coa –> reductase to mevalonic acid and acetoacetate
*cholesterol blocks mevalonic acid
mevalonic then goes to dimethylallylpyrophos and condense to farnesyl

then go to squalene (need 02) then lanosterol and cholesterol

79
Q

lanosterol and vit d

A

lanosterol makes vit d by cyto p450

80
Q

vit d effects

A
  • increases ca abs in bones and teeth?
81
Q

calcium is involved in

A

troponin c helps ca bind

- calmodulin bidns ca

82
Q

cholesterol fates 7

A

membranes, excretion product, bile salts, progestagens, glucocorticoids, mineralcorticoids, sex hormones

83
Q

bile salts

A
  • made in liver, store in gall
  • emulsify fats
  • polar so lots of OH groups added by cyto p450
  • from choles, needs nadph, coa to turn into glycine then glycocholate
84
Q

steroid hormones

A
  • found in endocrine tissue

- chols modified by p450 then pregnenolone and progesterone

85
Q

glucocorticoids

A
  • progesterone to corisol

- uses p450 and 21 hydroxylase

86
Q

glucocorticoid roles

A
  • increase in g6p activity
  • increase gluconeo
  • aa/ nuc synthesis
  • controls life of fibroblasts and lymphocytes
87
Q

mineralcorticoids and what they do

A
  • progesterone using p450 and 21 hydro to make aldosterone
  • ## reabsorption of na, cl and hco3
88
Q

androgens and estrogens

A
  • progesterone goes to andosterone and then estrone

testosterone then estradiol

89
Q

defect in 21 hydroxylase enzyme

A
  • means early puberty

- can’t make gluco and mineral so there is too mich sex hormones

90
Q

where do fa go after breakdown

A
  • go from intestine into mucosal cells
  • cholesterol goes in and some is amde into cholesterol esters
  • they clump together and form chylomicron
91
Q

chylomicron composition and structure

A
  • 2 protein, 85 tg, 13 cholesterol

- tg and ester are in the core, polar lipis and proteins are outside

92
Q

chylomicrons into liver

A
  • some tg is removed here by lipase
  • lp is then secreted with 2 new proteins of liver origin
  • called vldl
    10 protein, 50 tg, 40 cholesterol
93
Q

lipase digestion

A
  • attacks tg and chylomicrons and vldl

- complexed to serum albumin then broekn down or adipose

94
Q

lecithin cholesterol acyl transferase

A

cholesterol + phosphotidyl choline are turned to cholesterol ester and lysolecithin

  • toxic in high amts
  • combins in serum to form hdl
95
Q

hdl proteins

A
  • goes to liver to make phospho

- 50 protein, 50 lysophospho

96
Q

LDL protein

A
  • made from IDL, which looses a protein and becomes LDL
  • takes up by most tissues as a source of cholesterol (take receptor and ingest it)
  • the ones not taken up are picked up by macrophages
97
Q

familial hypercholesterolemia

A
  • heterozygous is 300-400 mg cholestol
  • risk of heart attack in 30s or 40s
  • homozygs is 600+ choles and heart in childhood
  • homo has no funcitonal receptors
98
Q

transamination

A
  • first step in AA breakdown
  • reversible
  • AA + Alpha ketoglutarate –> a keto acid + glutamate
  • need pyridoxal phosphate as cofactor (vit b6)
  • doesn’t happen unless low energy state
  • other transaminase can cut using aldolase and decarbo
99
Q

urea cycle

A
  • liver

- urea goes to kidney

100
Q

glutamate dehydrogenase

A
  • first step in urea
  • take glutamate + NAD to make alpha keto glu
    gtp and atp are -
    adp and gdp are +
  • in mito matrix
  • reverse reaction is very toxic
101
Q

other ways to get nh4+

A
  • ugh see card
102
Q

nh3 poisoning

A
  • drunken behavior

- give less protein and more ketoacid

103
Q

biotin

A
  • needed when co2 is added
104
Q

s adenyosyl methionine

A
  • transfers methyl groups

- uses n as an acceptor and methionine

105
Q

thfa

A
  • carbon in various oxidation states

- needs folic acid to become thfa by reduction

106
Q

vit b12

A
  • transfers alkyl groups from one carbon to another
107
Q

vit b12 problems

A
  • usually absobred in intestine
  • intrinsic factor binds it
  • pernicious anemia is when low intrinsic factor so no b12
  • treatment is b12 shots
108
Q

pyruvate AA pathways

A
  • ala, cys, thr,
109
Q

oxaloacetate pathway AA

A
  • asp a, asparagine
110
Q

path to alpha keto glu

A
  • glutamic acid, glutamine, argnine, proline, his,
111
Q

path to succinyl coa

A
  • met, threo, valine, iso leu and leu make using vit b12
  • do oxidative deamination
  • this leads to maple syrup disease if def
112
Q

phenylalanine + tyros

A

turns to acetoacetate

113
Q

leucine

A

ketogenic (acetyl coa + acetoacetate)

114
Q

tryptophan

A

gluco and keto

115
Q

lysine

A

ketogenic

116
Q

simple feedback

A

products blocks start

117
Q

sequential feedback

A
  • a has two paths where product of path inhibits start
118
Q

concerted feedback

A
  • a has two paths where the product blocks path AND a-

- need both to block a

119
Q

enzyme multiplicity

A
  • enzymes of pathways inhibit the pathway and the start of pathway
120
Q

cumulative feedback

A
  • lots of products made, and each increasingly inhibits the start
121
Q

covalent modification (glutamine synthetase)

A
  • amp binds to tyros

- gln synthetase without p is actie, when bound to amp it is less active

122
Q

aa uses

A
  • proteins, cofactors, hormones, porphyrins and heme, nucleotides, nt, pigments
123
Q

making porphyrin

A
  • start with delta aminolevulinate and condense using nh4+

- heme is negative effector???

124
Q

hemoglobin

A
  • 120 days
  • degraded by bilirubin, goes to liver to secrete with bile
  • high biliriubinn is jaundice
125
Q

acute intermittent porphyria

A
  • overactive aminolevulinate synthetase
  • high levels in liver
  • red pee
  • light sensitive
126
Q

hepatoerythropoeitic porphyria

A
  • one aa change for enzyme in heme to make unstable
127
Q

variegate porphyria

A
  • block in enzye leading to heme, so not enough negative effector heme
  • high levels of intermediates b4 blockage
  • need blood transfusions
  • light sensitive
128
Q

serotonin

A
  • made from tryp and pyrodoxal phos
  • sleep and memory
  • lsd thing
129
Q

dopamine and norpei

A
  • tyros
  • catecholamines
  • see card
130
Q

parkinsons

A
  • low dopamine

- broken down by monoamine oxidase

131
Q

melanin

A
  • dopa to red pigment then black
132
Q

pku

A
  • bad conversion from phenyla to tyros
  • converted to a phenyl pyruvate instead using transaminase
  • deficient in pigment
    , no protein formation

Exam Biology flashcards (11 decks)

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