BIOCHEM EXAM 3

thereinternetareremem
mitochondria are dynamic organelles
*
linkbetween glycolysis & citric acid
cycle in aerobic respiration thatc an form networks
pyruvate
-
dehydrogenase:
fates ofpyruvate:
blc they would scatter light

!underhypoxicconditions,pyrateisreducedpyruvatestransporterinone"erobic respiration RBC do NOTcontain

mitochondria blo
would consume the Oc they
were

mitochondrial matrix... subject regulation

to via
compartmentation they
& CAC occur in
PDH transporting
contain mitochondria
chemical run of PDH: 0
bacteria do NOT
= 33.5 k5/mol
0
Y-S-CoA +CO24"
-

Il
NAD+ HEC NADH
CrA-SH
-
+
-
-

Ha) -C-200
+
+

pyruvate acetyl-CoA Steps:Estance

acetyl-

Flexible
arm
neto utcome:
Ez dihydrolipoamide-E2
·hifrom Pererates, bondaretansterred nicester
to

E I
badat

res stabilized int. S

Haj
Step 1:El, using TPP cofactor, decarboxylates pyruvate,is -
drives wh
-200

ytatn mta I
Te
S on
CH3
-A-retent mantan 6H

nane
-> -
Hx
-
-

dis 7t
e Es
acetyl-dihydrolipramidetocoenzyme A **CH
-
-
R
3:Ez transfers acetyl group from
-

Step hydroxyethyl-
E2 0

reoxidize dis
Ha-ns-COA
3 -
SH NAS steps 415:E3 dihydrolipramide regenerate
to E2 then transfers e mobile NAD+
to

1- -
=o CoA-SH
+ ->
↳via redox-active disulfide bond adjacentto
tightly bound FAD
C coA 2 e, then transfers to NAD+to
acetyl thataccepts produce NADH
CH3 exchange one

thioester for another energetically favorable ble NADThas lower reduction potential
increase
to effective conce
channeling":covalenttethering
of "substrate pairs of e- up in ETC
PDHgreatexample ~I
end
Citric Acid Cycle
toxic intermediates
& protects against
e

3NADt+FAD+GDP+Pi 2H.OF 2COc 3NADH FADH, +GTP+2H++GoA

+

Acetyl-CoA
+
+
+
cell
energetic needs oft he
according to
PDH regulation: 2 C from acetyl-coAoxidizedall the
way CO2
to

Acetyl-CoAinhibits
-

feedbackinhibition ->
via NADH & acetyl-CoA
⑧

I allosterically Il
PDH
also if low Oc levels, won'tb e running CH3-C-S-COA& condensation
CoA-SH
② covalentmodification of E I ->
reversiblephonewitha energy ⑧ dehydrogenation ↳ Wi
H20

HO-cH-YDtecatnaseYCH,-100-
EI active
dephos
=

activated via
Mgrt, Cat, insulin inhibited via
pyruvate, ADP

recenton into
blood ⑦ hydration cit -200 -

dehydrogenase
sugar
HCO fumarase - malate
in
③ transcriptionally
HC-200-
drain
cycle step-by-step
tricarboxylic -002--H fumarate
CA
-
oneratetoform strated CH2-100-

orea-ketoyintractor
to
attaches acetate
Ocitrate synthase
form new
used to cis-Aconitate
- 100 -

coupled
-> to
hydrolysis ofacetyl-CoAis "H-100-
C-C bond, acetyl group pathway
commits to

driving force for laststep ofren

A CH2-C00succinate
firstcommited step:highly regulated

② aconitase isomerizes citrate

to isocitrate
alcohol,
aconitase/naration
3 to
2 to make ita secondary CH2-208-
-hydroxyl from position
oxidize
which is easier to

makes this run "go by the flow" t

a-ketoglutarate
change
-

small free energy SUPER

CHc-100 dehydrogenase
mare
iron sulfur cluster orients enzyme active siteto

-coi
complex
of isocitrate CUA-SH
Stereospecific chiral 2R,35 diastereomer
dehydrogenase
③ isocitrate catalyzes firstenergy-harvesting step ③ oxidative
p-ketogroup which is super
unstable & 900- ! con"QUAD+ CO2 decarboxylation
strategy oxidize ditc
to
to
& NADH
is a good (G... spontaneously degrades
into
d-ketoglutarate
NAD+as
2e- go to
A
a
hydride key regulation step
harvesting et NADHGylation, coo

aetoglutarate dehydrogenasecatalyzesanother
⑧ energy
omplex
E3 identical, El&E1 slightly
differentsince noswinging arm
ation of
-
C.A. cycle
much larger molecule than pyruvate
substrate
so active site accommodate
must
as a whole
is key
availability
substrate
force in
regulating
serves as redox sensor mitochondrial functioning inhibition
HIGHLYregulated run, in fact to
&
·allosteric feedback
ALL steps
⑤ succinyl-CoAsynthetase uses energy of succinyl-CoAto mare ATP/GR
energy charge regulates virtually
substrate-level phosphorylation of NADH findan
=

phosphorolysis followed by hypoxic conditions build up

-

⑩ dehydrogenase
succinate
an alkene, transferring ze-to
oxidizes (-(bond to
FAD
costlycoo_dorteta much inhibitors NADH, ATP,
=

Acetyl-CoA, succinyl-CoA
succinate:stronger oxidizing agentneeded FAD
Enz-FADHE comated to activators:ADP, Ca2+
=

pull outa from

hard to
En
ofETC
transmembrane protein,
part -
sets of oxaloacetate
regeneration
& pulls some e- outi n meantime NADH
hormone regulation:
up
oxidizes fumarate
to malate
activators:Mg, Cart, insulin, ADP, pyruvate
⑦ fumarase stereospecifically
double bond indirectregulation ofS.A. cycle involves -

hydrates intermediates
deplete
·Enterpresses
they can move across mitochondrial membrane ->

fumarate have
& malate transporters so
buildup intermediates
metabolic pathways other
and interface with
NO LOSS OF ENERGY
shuttle
cartate
extracting energy tally:1mole glucose
*

ex. malate as MDH enzymes

-

transaminase &
cytoplasmic NADH (glycolysis)
ETC using *C.A.cycle
mitochondria:2 ATP, 8 NADH, 2 FADH2
into
"Shuttle"for getting e-from
oxaloacetate
⑧ malate oxidatively
dehydrogenase regenerates
triple rxn: double bond formation, hydration, & NAD+ -
dependent dehydrogenation cytoplasm:2ATP, 2 NADH -glycolysis
1G" =29.7k5/mol:unfavorable in standard conditions
+

i s presentatSUPER low cone. Since

drivenby conc. dep. factor bloxaloacetateof C.A.cycle
gets immediately consumed by firststep
shuttle
another ex. of shuttle is glycerophosphate in the
prose
but loses a little energy
cytosolic NADH into ETC,
FEH
 Transport generatesaman reachpotentElegant, ImosesininEmera"more positive dontratecenters cytochromes heme-
are
Electron A
-

redux-active containing proteins, can

in order
keep reducing, need stronger a
stronger agent transfer e-using their
1G"=-nF)Eacceptor Econor)
to
E not
-

hungryfore- -

III central iron ion

Complex
=

reductase) uses"&cycling"
+
E very
=
hungry fore- dehydrogenase)
Complex I [succinate CQHz-cytochrome c

↑CH
sulfur clusters thencyte
affinity
Iron
ComplexI districtaboute ALWAYS single etransfer
succinates high to
feltocytes, cyte e-tocyte,

Testineverge -- -
then

paten"8x states
inoxgenerainstreduced
Fert-Fest needed,
oxidant

environmenti n which these are

protein
can
clusters are in in a thus

essential
widely vary the reduction potential treated starveoutemping oxidase)
Vitamin B2 ComplexIN (cytochrome c

· fremetsrati bir mediates

o
i
paththroughnemesincenterahigh?
inhibitors of ETC:
protectedcompetence agare inhibits complexII
antimycin A: &
& the
the Nat/A antiporter cycle 2 H20
reduce O2 to
homologous to to

rotenone:inhibits transfer of e-from

cits found via
complex I
toQ intermembrane space
IOHttransported into
this pathway was
NADHmolecule
per

↳
OH reveanaein in mito.memb.
associate
respiratory complexes
*

x cyt, cytc cyt(a as) 02 to form "supercomplexes"or "respirasomes"

cytb
- - + -

efficiency
-

NADH Q channeling promote

-
to

likely function:substrate
-

payment I
cring
-

rotor: 7, 8, 9 subunits

i n
+

its
ubiquinone (A)
ubiquinol (AHz)

Fort h e
reduced
oxidized all rotate
do rotate
stator+dB-subunits
irriatricemiagiarist
not

-
-> LARGEreservoir of
potential energy
inserts into
Y subunit

show
coiled coil
has make, thus
energy to
not
central of
cavity C, complex
total:v2.5 ATP perNADHhowever F, complex
perfectly essentianI
good

mechanism: matrix
subunit allow for passage of Hindirectly
on

I half channels in a side

favorable for Ht driving conformateat
are/imnigtanginscriptominbunit
rotates
pH (lots ofHt)
on intermembrane side
lower

↳etecting harnes,areinlongerine
release
to
of other
itout half channel tomatrix
- -
-
tightAone full rotation (360%
of ysubunitproduceatalytioman
Ht down EC gradientCOUPLED endergonic
to ADP-4 ATP is

Summary:exergonic Pi
+

residue thus
ATP synthesis inhibitor: oligomycin-binds to curing critical Glu
matrix
backt o
flowing
experimentalhed
H+from
& synthesis ATP preventing too steep keepto
pushing
to pat againstgraceitbecomeswhich inhibits
coupling of ETC, proton gradient, availability
substrate
linked to
->
found this outbicon is stoichiometrically ETC C.A.cycle
cost associated my running
then NADHbuilds up if ETC
running
isn't
if ATP can'tbe made, ETC stops. Why? reactive O2
&
PDH burns up fuel generates &
deadly banned by FDA
shows justhow finetuned
this process is of cellular respiration
uncoupling ATP synthesis from ETC via DNP-firstdmg respiratory control" -

*(ADP) this SPEEDS UP system

DNP binds protons & transports back
matrix
to thus dissipating if

the protonmotive force wo ATP synthesis Glucose CO2 32 ATP produced for plants => =

keeping score
tissue
the case of brown adipose
are
in
= 6-6 ATP 2NADPH
regulated uncoupling can be useful in

uptime wrote waveorourgranite pimicmolecules

~
2H20 27Y
hibernating efficiency =

mammals et
membrane
Photosynthesis
- (lightreactions)
-
Tumend
doesn'tlose
built, absorb granum
energyfor his
-
PSI firstexcitation, includes many pigmentmolecules
D1&D2 are ran center subunits, p488:special pair of chlorophylls goesincenting.Also
10-100 picoseconds,
res, transfer of
till reaches
plastoquinone blot w/ x 680nm
"(y+blf ->P700 center
=

P680 pheophytina QB cytochrome

-> run
Planin (PSI)
-

↓PSI
PH+
per split H20 thylakoid lumen
into
pumps to PSI
oxiding agent, oxidizes H20 (like Complex III) via plastocyanin
P688 (e- deficient) Biology's strongest using &cycling ulation mechanism:
+

-using cucenters
-

ferredoxin & Fesclusters A Fd sends

-

from PSI
ifcell has enough NADPH,
n e

=
to
PSI e-from plastocyanin

terryeskritrate
E protein: ferredoxin-NADP reductase undergoes this rxn:
backt o cytblot, translocating HT, making more ATP
transferring
de
-

2H*
+
+
2NADP+=ZNADPH 2, 1 ata -> helps to balance
ATP & NADPH production
time
based on needs of cell (such as for dark rans)

innonaneareininairesagraceen
permeable

immro.ca) tuoo+
than
H

a
Ruleintermediate th
BiscO-Psymmustabundant
OEC 6.
-> redox-active Tyr
key 4486t
residue shuttlese to
-

(thus requires et enediolate carboxy-p-keto

intermediate, then
Calvin Cycle process reductive a 3PG's
might
fixtarbonsynthesize carbohydrates
in a
before splitting
into &
to GNADP+ + 3 H2O utilizes carbamylated lysine
GH+-CH00s-phosphate 9ADP+8Pi active site
+
+

9AM GNADPH
+ ->
enzyme
attach CO2
strongly
+

3CO2+ -
to
via T.S.
transition state
late some selectivity
->
stabilizes croducti n order have to
ofcalvinkinases
to

nation are the regulated set the

resembling over O2, butthis
between
leads "T.S. inhibitiont
& selectivity
speed
RuBP CO2+H2O,2 3PG
+
body reaches
a compromise
↑pH ↑activase
↑mg2tFd OCA1P
 need 3 RUBP 's ( Sc) to keep cycle going
convert 5 GAP 's ( 3C) to
glycolysis)
to
3PG to GAP (steps 647 of
② reduction of
-

/
RUBP ( co ,
1,3 BPG cleavage of acyl phosphate ③ regeneration of acceptor)→ odd " "
3pct A GAP
-

TIM ( isomerase)
-

drives
bond
A gap = DHAP via
rxn
2 ketoses -

NADPH NADP
-1
ADP
Afp Pi 1- ketose & 1 aldose = 6C
aldolase combines
+

RUBP
regeneration of + 4C E4P
-

5 to to aldose acceptor → 5C
ketose
GAP , / need 23C molecules to
make 91"'
trans keto age takes 2C from
3 coz's go through cycle producing
,
6 -

11 to carbohydrate synthesis aldolase adds zc ☐ HAP +4C E4P

→ 7C SBP

to make 2 last 5C molecules

trans keto lase transfers 2C from TCSBP to GAP
to regenerate 3 RUBB
amylose
sucrose RSP & 2xu5Ps are converted to 3 Rugps
4
phosphorylated
made in Rust
made in 4 t'
stroma cytoplasm 3 Rust 3 RUBP
isomerase epimerase A ,

3ATP 3 ADP

like reverse
of Calvin cycle
Pentose Phosphate Pathway
-
oxidizes glucose in cytosol kinda ,

-
CNADPH how humans mare
←
NADPH of NADPH =
protecting
stores reductive power in *
important use
'

synthesis damage via

"

for nucleotide & A. A. oxidative

generate sugar phosphates cells from cellular weapon
i
"

(from nucleic acids ) reduction of glutathione ←

to metabolize dietary pentoses
are hypersensitive
-

→ happens in
anabolic tissue , making
oxidative
fat
phase 6- PG
y, Guppy activity
stress ✗ ① ""
"
¥ "" " "
stage "1" NADPH production to oxidative amylose
:
:
glycogen /
) w/
amylopectin till@
'¥"Ee phospho gluconate Ai RUSP -
starch -14
gyp 6- phospho glucono
lactone -

used to speed plants store glucose

as \
(1-26)
Ai
NADPH of G6PDH
Appt NADPH
UP dough rising 4. amylase s cleave ✗ (1+4) branch points
24 -30 residues
✗

* inhibition
.
Napp + CO2
Rub P] during
Ht
When I [NADPH ] but
low [ make DNA in commercial maltose units every
+

cell division to & releases

bakeries
small intestine
.

cells : non oxidative phase

based on needs of 6) in
glucosidase cleave all
-

: shuffles carbons
stage 2 1 GAP which can both go through glycolysis then , n°0 -
limits
all 6) branches
: converts to 21=613 &
in cell
not much needed side chain
,

Rugp
animals store glucose as glycogen
.

u5PÉr GAP in 0 cofactor , catalyzed by lysine molecules

hrensesdtabbiutizsdhitctarbbaanion
Rust ← ✗
contain to -90 glycogen

(
glycogen granules
:
SMP after cleavage molecule
✗ USP per glycogen
rasp 2000 non reducing ends
exportable energy
.

transketolase uses TPP as cofactor ~

glycogen for
-
12-29 hrs
liver contains not of wet weight
GAP =

Rsp trans aldolase

weight of glycogen
.

ugp transketolase ~ , -2% of wet

& adapt to needs of cell skeletal muscle contain \
usable energy
be very versatile
branch points allow for this pathway to for 4hr

buildup of glycogen (requires energy

)
NADPH
Glycogenesis phosphatase
:

synthesis well as
needed for nucleotide as
energy) followed
- by pyro
,

breakdown of glycogen ( does

NOT
require ① UDP-glucose pyro
phosphorylase - ,

Glycogen olysis + Ppi

:

① glycogen phosphorylase
T-rex GIP + UTP # UDP-glucose of rxn)
point
=

4 ends until units from branch driving force

zpi (hydrolysis
~
non reducing
=

✗ (1%4) linkages from Pi & releases each unit as GIP

-

ppi an ATP
cleaves
requires regenerate UTP costs
using phospho wlysisdiffuse abundant ATP indef
,
+1,0 to
:

breaks bond celt of existing glycogen

.

out of which is always

linear enlargement
'
can't just via Schiff base @ Lys
680
does this so glucose
② gnyogengyntnage
:
body bound to enzyme ends
PLP cofactor (✓ it Bu) covalently canola clone mimics
intermediate
reducing
enzyme requires for .mg ✗µ g) bond @
-
non
carbocation intermediate inhibitor =
1,5-914
UDP + glycogen +1
,
mech undergoes & partial positive charge
notice positive
.

UDP-glucose glycogen molecule

+

¥¥÷µ+
o
, '
@ center of each glycogen IS
C2 enzyme
sym\ glycogenin protein
OH inh
transferase substrate
.
= :

int
& d- 1,6 glucosidase catalytic tyrosine glycosylin
-

transferase
.
-

② de branching enzymes auto unit

=

glucose
-

end of chain
glycogen
o=

transferase transfers 3 units to non

-

reducing in
point releasing glucose glycogen O 00000000
remaining all 6) branch Hupp Tyr
-
-

cleaves last
Tyr OH
,
a -1,6 glucosidase -

pathways VDP
-

off substrate in dif -

converts GIP to GAP to as

gµµge
③ phospho glucomutase go
.

phosphate exchange branching

enzyme introduces chain
phosphorylated serineto enzyme participates
in
③
:

mutase there is was His res W/ ④

on
branching
yield 7 unit
phosphoglycerate (1%4) to
glycosyl unit
-

→ glycolysis analog of regulation)

,
cleaves ✗ &
net hydrolysis (feature between 7 unit chain
6) bond forms
since no
reaction is reversible or PPP
before use in glycolysis g. ( µ (1*4) more
favorable b/c breaking
,
✗
on needs)
* glucose must be phosphorylated can occur (depending
GUP phosphatase energetically ,, g)
But in liver Gyp glucose using favorable than ✗ ,
stimulates anabolic pathways glycogenesis
, + -

of glycogen metabolism fed state → insulin

Regulation stimulates catabolic pathways glycogen
olysis

hopatÉ
→
b to activate
of glycogen synthase
starved state
→
glucagon dephosphorylation PPI
glycogen synthase
a via
to make AMP
regulation
•
adenylate cyclase reciprocal
activates GPCR stimulates glycogen synthase
=

pka inhibits
glucagon kinase A ( PKA) 1 of
camp activates protein
cascade activates glycogen phosphorylase
(step ) allosteric activation t[G6P]
glycogen lysis disturbs blood sugar homeostasis
,

phosphorylation mutase Mh glycogen storage

diseases =

determines direction of phospho 91400 's disease G6 phosphatase deficiency

[Gap ] von Gierke
=

tasted state
fed state GUP to blood glucose
break down
t[G6P] → GGP via glycogen olysis can't unbranched chains .to#akdown
T[G6P] → GIP via glycogenesis Andersen, disease
=
very long
T-rex isn't working
fÉ9. McArdle's disease
-_
gly phosphorylase
.

in muscle cells
,

liver
occurring primarily in
gly phosphorylase T-rex isn't working
net reaction
glucose -14 ADP +2GBP -1613-+2 NAD Hers
-1 = ,
disease
: '

+21-1++61-120 → liver cells

.

in
ATP 2 GTP + ZNADH
2. pyruvate +4
opposing pathways ?
+

acid oxidation favor

from lactate
→Tgyvia fatty HOW does body
kinetic control → controlling enzyme activity
,

breakdown answer :
lipid & protein
opposite rxns regulated glycolysis in are regulated in
gluconeogenesis
exercise
PEP undergoes reverse glycolysis until F- 1,6 BP
-

in multiple organs
& tissues during
The Loricycle occurs LDH
pyruvate to glucose to then be broken
down
again via
interconverts lactate to -1 Cata lyres reaction of PFK -1
2 FBPase
reverse
Pyruvate carboxylase Bypass :
peper
1 PEPCK + .

Bypass forward
:
"
malate OAA # PEP hydrolysis ester drives rxn
OAA malate energy of phospho
pyruvate -1
NADH GTP GDP
phosphorylate & of vxn in the cell
) kinetic control direction sci -15.9kt / not
NAD to
using this energy
, "
NAD
NIFF
,
Hcoj + Pi + Ht
de carboxylate OAA
'
+ ,

ygpt-kj.jp
=

acetyl-CoA
maaspartaeH-
=

will use these coz LG same as one

(
allosteric activator by PC
e- to run GADPH that was added F 613
¥, F- 1,6 BP
-

residue acts as
Biotin cofactor covalently attached to Lys -
,
in reverse ,
carboxyl carrying -16.3kt 1m01
¥÷e¥
-
"

intrans ported to liver when glucose is 10W prosthetic group swinging transfer CO2 from 1-1105 pyruvate SG
"
"
-

arm to to =
?⃝
 3:Glucose-6-phosphatase -- makes glucose exportable (GLUT2 & nexokinase IV)
Bypass gincokinase
lowsite... only enters cytosol very high
↓
levels in are
localized in liver ER, compartmentalized b/c enzyme is promiscuous exitc ell glycolysis if glucose
a transmembrane helices, transporters for Glep
& Pi
formed glucose is protected from ↳reciprocal regulation
facing the lumen, so newly
subunitup active site
catalytic
glycolytic enzymes
in
cytosol

Mcercoterter
in
bypass enemininegenes
t
regulation F-1, 4 BP
hormonal ↑ -

to
PFK-2/FBPase -
2 subject
via phosphorylationwhich
insulin activates PP1 dephosphorylates O acetyl-crA
- in the kinase domain
PFK-2/FBPase 2, resulting
Pase-1
F-b ⑧ alanine
& PK are subject
- -

F-2,4-BP

Feel liver, PEPCK

being active, producing in

·29EeipPriptnnuriphoslaus
via
XAMP hormonal regulation
to

relieves inhibition
of phosphorylation
active, b [F-2,6-BP] direction
FBPase-1 which drives ran in gluconeogenic