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323 Cards in this Set

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complexes in etc
I
II
CoQ = ubiquitin
III
IV
V
complex 1 aka
nadph dehydrogenase
complex 5 aka
atp synthase
location of etc
mitochondrial membrane
e's from nadh and fadh2 are transferred to.....
ubiquitin
complexes containing Fe
3 and 4
atp synthase
complex 5
complex that needs cu
4
complexes containing heme groups
3 and 4
complexes with ability to pump H+'s to intramembranous space
1
3
4
complex which allows H+'s to be pumped across matrix
5
how complex 5 creates ATP
uses gradient from H+; it has a proton channel that allows for protons to cross into matrix
atp yielded by nadh
2.5 atp
atp yielded by fadh2
1.5 atp
how does complex 4 create h20
e-s are transferred to 02, which combine with h to form h2o
ubiquitous: hexokinase or glucokinase
herokinase
found only at liver and pancreas: hexokinase or glucokinase
glucokinase
allosteric activator of glucokinase/hexokinase
insulin
allosteric inactivator of glucokinase/hexokinase
glucagon
high affinity: hexo or gluco kingase
hexokinase (low km)
low affinity: hexo or gluco kinase
glucokinase (high km)
high capacity: hexo or glucokinase
glucokinase
no feedback inhibition: gluco or hexokinase
glucokinase
phosphorylates excess glucose after a meal to sequester at the liver
glucokinase
energy source of brain: N, under stress, and under extreme stress
N - glucose
stress - glucose
extreme stress - ketones
energy sources of heart
N - FFA
stress - glucose
extreme stress - glucose
energy sources of muscle
N - glucose
stress - FFA
extreme stress - FFA
energy sources of rbc
N - glucose
stress - glucose
extreme stress - glucose
always seen with disrupted glycolysis? and why?
hemolytic anemia bc glycolysis is the only source of energy for the rbc
glucose -> g6p
glucokinase (hexokinase)
g6p -> f6p
g6p isomerase
f6p -> f1,6dp
fructose 6 phosphate kinase = pfk1
f6p -> f2,6dp
f6p kinase
f16dp splits into.....
dhap and g3p
cuts f16bp into 2 3 c molecules
aldolase a
conversion bt dhap and g3p
triose phosphate isomerase
g3p -> g1,3bp
g3p dehydrogenase
g1,3bp -> 3pg
phosphoglycerate kinase
3pg -> 2pg
mutase
2pg -> pep
enolase
pep -> pyr
pyruvate kinase
pyruvate -> AcoA
pyruvate dehydrogenase
site of glycolysis
cytoplasm
blocks enolase
fluoride
net glycolysis:
Glucose + 2pi + 2ADP + 2NAD+ -->
2 pyruvate + 2 atp + 2nadh + 2 H+ + 2h2o
complexes in etc
I
II
coq
III
IV
V
nadph dehydrogenase
I
only complex that's not a protein
coQ
complexes where H+ is formed
I
III
IV
ATP synthase
complex V
directly inhibit electron transport
electron transport inhibitors
causes of low proton gradient and block of ATP synthesis
electron transport inhibitors
directly inhibit mitochondrial APTase
ATPase inhibitors
causes an increased proton gradient, but no ATP is produced because electron transport stops
atase inhibitors
decreases permeability of membrane
uncoupling agent
causes decreased proton gradient and how o2 consumption
uncoupling agents
atp synthesis stops, but electron transport continues
uncoupling agents
internal combustion
uncoupling agents
inhibits complex I
rotenone
amytal
inhibits complex II
malonate
inshibits complex III
antimycin
inhibits complex IV
co
cn
chloramphenicol
inhibits complex V
oligimycin
complexes with heme/Fe
complex IV and V
uncoupling agents
DNP
Aspririn
UCP
chemiosmotic theory
e- transport causes H+ ions to be pumped from matrix to intermembrane space, resulting in pH and electrical gradient. energy created harnesses atp formation, as protons travel down gradient into matrix through atp synthase
in energy investment phase, 1 glucose becomes ?
2 G3p
# of atp consumed in glycolysis
2 atp
rate limiting step of glycolysis
fructose 6 p -> fructose 1,6 bp via PFK1
# pyruvates yielded by glycolysis
2
atp produced at what two steps of glycolysis?
PEP -> pyruvate via PEP pyruvate kinase and
g13bp ->3pg via g13dp kinase
step that drives glycolysis
PEP -> pyruvate
nets 2 atp
step of glycolysis that yields nad+
g3p -> g13dp via g3p dehydrogenase
mercury poison inhibits this step of glycolysis
g3p -> g13p via g3p dehydrogenase
can be used in glycolysis, triglyceride synthesis, and with G3p shuttle (glycerophosphate shuttle)
DHAP
allosteric activator of PFK
fructose 2 6 biphosphate
insulin
amp
allosteric inhibitor of PFK
glucagon
atp
citrate
glycolytic enzyme deficiency causes....
hemolytic anemia
irreversible enzymes of glycolysis
glucokinase
PFK
pyruvate kinase
pyruvate dehydrogenase
reverse process of glycolysis
gluconeogenesis
irreversible enzymes of gluconeogenesis
pyruvate carboxylase
PEP carboxykinase
fructose 1,6 bisphosphatase
glucose 6 phosphatase
in energy investment phase, 1 glucose becomes ?
2 G3p
# of atp consumed in glycolysis
2 atp
rate limiting step of glycolysis
fructose 6 p -> fructose 1,6 bp via PFK1
# pyruvates yielded by glycolysis
2
atp produced at what two steps of glycolysis?
PEP -> pyruvate via PEP pyruvate kinase and
g13bp ->3pg via g13dp kinase
step that drives glycolysis
PEP -> pyruvate
nets 2 atp
step of glycolysis that yields nad+
g3p -> g13dp via g3p dehydrogenase
mercury poison inhibits this step of glycolysis
g3p -> g13p via g3p dehydrogenase
can be used in glycolysis, triglyceride synthesis, and with G3p shuttle (glycerophosphate shuttle)
DHAP
allosteric activator of PFK
fructose 2 6 biphosphate
insulin
amp
allosteric inhibitor of PFK
glucagon
atp
citrate
glycolytic enzyme deficiency causes....
hemolytic anemia
irreversible enzymes of glycolysis
glucokinase
PFK
pyruvate kinase
pyruvate dehydrogenase
reverse process of glycolysis
gluconeogenesis
irreversible enzymes of gluconeogenesis
pyruvate carboxylase
PEP carboxykinase
fructose 1,6 bisphosphatase
glucose 6 phosphatase
pathways occuring at both cytoplasm and mitochondria
gluconeogenesis
urea cycle
heme synthesis
rate limiting enzyme of gluconeogenesis
pyruvate carboylase
rate limiting step of gluconeogenesis
pyruvate -> OAA
via pyruvate carboxykinase
pyruvate -> OAA
pyruvate carboylase
OAA -> PEP
PEP carboxykinase
F1,6BP -> F6P
fructose 1,6 bisphosphatase
g6p -> glucose
glucose 6 phosphatase
biotin and ATP requiring
pyruvate carboxylase
pyruvate carboxylase's allosteric activator
AcoA
pyruvate carboxylase's allosteric inhibitor
glucose, adp
gluconeogenesis enzyme requiring gtp
PEP carboxykinase
enzymes found only at liver (90%), kidney, int. ep., adrenal cortex (10%)
Pyruvate carboxylase
PEP carboxykinase
F16bphosphatase
glucose6phophatase
explain how OAA is shipped from the mitochondria to the cytoplasm in gluconeogenesis
Pyruvate is in cytoplasm
Pyruvate -> OAA is only step occuring at mitochondria
OAA -> Asp via AST
Asp can cross membrane to cytoplasm.
Asp -> OAA via AST
OAA -> PEP
only step of gluconeogenesis occuring in mitochondria
pyruvate carboxylase
deficiency of key gluconeogenic enzymes causes....
hypoglycemia
steps of gluconeogenesis
pyruvate -> OAA *irr.*
OAA -> PEP *irr.*
PEP -> -> -> f16biphosphate
f16biphos -> f6phosphate *irr
f6phos. -> g6 phos *irr.*
g6phos -> g6p *irr.*
vitamin needed with transaminases
B6
viral hep ast:alt
<2:1
alcohol hep ast:alt
>2:1
hepatic necrosis ast:alt
>1000
Steps of N galactose metabolism
1. Galactose -> Gal-1-P via GALACTOKINASE (requires atp)
2. Gal-1-P -> UDP-gal + Ph. via UDP-gal + Uridyl transferase
3. UDP-gal -> glu-1-ph via Epimerase
4. glu-1-ph -> glu-6-ph via Mutase
5. glu-6-ph -> gluconeogenesis/glycolysis
galactose -> galactose-1-ph
Galactokinase
sugar carrier of galactose metabolism
UDP-glucose
galactose -> galactitol
aldose reductase
gal.-1-pph -> udp-gal + ph
udp-glucose + uridyl transferase
udp-gal + ph -> glu-1-ph
epimerase
glu-1-ph -> glu-6-ph
mutase
absence of galactose-1-ph uridyltransferase
galactosemia
inheritance of galactosemia
AR
deficiency of uridyl transferase builds up....
galactose-1-ph
galactose
galactitol
(toxic to parenchymal cells of kidney, liver, lens, spleen, and brain)
tx of galactosemia
eliminate lactose and galactose from diet
screening of galactosemia
+ reducing substance when pt given milk
cataracts + jaundice/hs + mental retardation + poor feeding
galactosemia
galactitol buildup
cataracts/neuropathy
benign: galactokinase deficieny or uridyl transferase deficiency
galactokinase
inheritance of galactokinase deficiency
AR
function of galactokinase
to phosphorylate galactose into galactose-1-ph in galactose metabolism
builds up with galactokinase defiency
galactose and eventually galactitol at lens of eyes
enzyme that causes galactitol buildup
aldase reductase (galactose reductase)
usually the sole manifestation of galactokinase deficiency
cataracts - infants
monosaccharides
glucose
galactose
fructose
ribose
disaccharides
lactose
maltose
sucrose
glucose + galactoase
lactose
glucose + glucose
maltose
glucose + fructose ->
sucrose
fructose -> f-1-p in fructose metabolism
fructokinase
f-1-p -> ? in fructose metabolism
DHAP
glyceraldehyde
other metabolic pathways shut down by fructose intolerance
glycolysis (thru glyceraldehyde-3-p)
gluconeogenesis (thru glyceraldehyde-3-p)
glycogenolysis (thru glyceraldehyde -> glycerol synthesis)
essential fructosuria
defect in fructokinase
heredity of essential fructosuria
AR
symptoms of essential fructosuria
usually, benign assymptomatic and incidental finding;
fructose appears in blood and urine
tx of essential fructosuria
not necessary
fructose intolerance
hereditary deficiency of aldolase B
inheritance of fructose intolerance
AR
accumulates with fructose intolerance
fructose-1-p
decreased pathways with fructose intolerance
glycogenolysis
gluconeogenesis
glycolysis
glucose + fructose
sucrose
treatment of fructose intolerance
decrease intake of fructose and sucrose (fructose + glucose)
symtoms of fructose intolerance
low energy state, jaundice, cirrhosis, vomiting, kidney failure, pt. assymptomatic until feeding fructose or sucrose (table sugar) at 6 months
low energy state + decreased inability of 6 month old to take table salt
fructose intolerance
least likely sugar to turn into glucose and why
fructose - because feeds into glycolysis after RLE, PFK-1
highest rate of metabolism of sugars
fructose
describe ethanol metabolism
*ethanol is a fate of pyruvate
ethanol -> acetaldehyde via alcohol dehydrogenase
acetaldehyde -> acetate via acetaldehyde dehyrogenase
what happens to NADH formed in ethanol metabolism
NAD fools the body into thinking there is energy, but actually the NAD isn't in the mitochondria so no energy can be made.
sx of NADH buildup in alcoholic
tricks body into thinking it has energy; but actually -
low energy state, hypoglycemic
high NADH/NAD in liver causes conversion of.....
pyruvate -> lactate
OAA -> malate
responsible for hepatic fatty change in alcoholics
high ratio of NADH/NAD+
finding at liver with alcoholic
MACROSTEATOSIS (liver takes longest to break down - shunts away from glycolysis) then
CIRRHOSIS(low albumin, high PT, high estrogen)
alcohol dehydrogenase
ethanol -> acetaldehyde
acetaldehyde dehydrogenase
acetaldehyde -> acetate
drugs with anabuse rxns
metronidazole
cephalosporins
mechanism of antabuse
inhibits acetaldehyde dehydrogenase and acetaldehyde accumulates, contributing to hangover
kinetics of alcohol dehydrogenase
0 order kinetics
buildup of formic acid...this buildup could cause blindness
methanol - an alcohol
an example is antifreeze, which can make oxylate kidney stones
ethylene glycol - an alcohol
5 fates of pyruvate
lactate (anaerobic)
alanine (anaerobic)
ethanol
AcoA
OAA
enzymes leading to 5 fates of pyruvate
->lactate = l. dehydrogenase
->ala = ALT
->OAA = pyruvate carboxylase
->AcoA = p. dehydrogenase
-> etoh = ?
builds up during anaerobic metabolism to save from lactic acidosis
alanine
provides NAD+ needed for g3pdh
Nad+ formed by LDH
pyruvate -> lactate
anaerobic fates of pyruvate
lactate
alanine
aerobic fate of pyruvate
AcoA
LDH for heart
1
LDH for muscle, rbc
2
3
LDH for liver, lung, kidney
4
5
liver enzyme that shows up earlier - 2 hours
troponin I
liver enzyme comes at 6 hours
ckmb
liver enzyme that comes in 24 hours
ldh
requires biotin for cofactor in 5 fates of pyruvate
pyruvate carboxylase
requires TPP cofactor in 5 fates of pyruvate
pyruvate decarboxylase
uses cori cycle in 5 fates of pyruvate
lactate
6 atp's that are needed to generate glucose from pyruvate
1. Ala carries amino groups to liver from muscle
2. oaa can replenish TCA or be used in gluconeogenesis
3. transition from glycolysis to tca cycle
4. end of anaerobic glycolysis
major ending pathway is pyruvate for these sites
rbc
leukocyte
kidney medulla
lens
testes
cornea
end of anaerobic glycolysis
pyruvate -> lactate or
pyruvate -> alanine
enzymes for 5 fates of pyruvate in cytosol
ldh, ALT. pyr decarboxylase
enzymes for 5 fates of pyruvate in mitochondria
PDH
PC
causes backup of pyruvate and alanine, resulting in lactic acidosis
pyruvate dehydrogenase deficiency
only a.a's that don't stimulate lactic acidosis
purely ketogenic a.a.'s - lys and leu
how one gets pyruvate dehydrogenase deficiency
congenital or
acquired - alcoholics due to b1 deficiency
findings of pyruvate dehydrogenase deficiency
neurologic defects
treatment of pyruvate dehydrogenase deficiency
high intake of ketogenic nutrients (high fat content or high lysine and leucine)
lactic acid buildup causes
stimulates GABA
denatures proteins
hyperkalemia
transfers excess reducing equivalents from rbc's/muscle to liver, allowing muscle to function anaerobically
cori cycle
enzymes in pyruvate dehydrogenase complex
1. alpha keto glutarate dehydrogenase
2. branched chain aa dehydrogenase
3. pyruvate dehydrogenase
cofactors needed for pyruvate dehydrogenase complex
TPP
Lipoic acid
CoA
FAD
NAD
vitamins needed for pyruvate dehydrogenase complex
first 4 B vitamins + l. acid=
b1 = thiamine
b2 = riboflavin
b3 = niacin
b5 = pantothenic acid
lipoic acid
order of axn of cofactors in pyruvate dehydrogenase complex
"tender loving care for nancy"
Tpp, L. acid, CoA, Fad, nad
Tpp's reaction
decarboxylase (-co2)
Lipoic acid's reaction
accepts acetyl groups
CoA's reaction
final acetyl acceptor
Nad's reaction
oxidizes fadh2; nad+ takes fadh2's e's
Fad
oxidizes lipoic acid -> fadh2
highest delta G of pyruvate dehydrogenase complex
nad
deficiencies of each cofactor of pyruvate dehydrogenase complex
thiamine -> wernike's encephalopathy or beri beri
l. acid/ p. acid -> none
Niacin -> pallegra
riboflavin -> angular cheilosis
overall reaction of pyruvate dehydrogenase complex
pyruvate + nad+ + coA -> AcoA + co2 + nadh
inhibits lipoic acid
arsenic
arsenic poisoning
arsenic -'s l. acid:
vomiting
rice water stool
garlic breath
pyruvate dehydrogase complex catalyzes what reaction?
pyruvate -> AcoA
seen on lab of pyruvate dehydrogenase deficiency
high lactate/ high pyruvate levels
lactic acidosis
lactic acidosis + neurologic deficits (developmental delay, abnormal muscle tone, seizure)
pyruvate dehydrogenase deficiency
pyruvate dehydrogenase if rle for....
kreb cycle
location of TCA cycle
mitochondrial matrix
fuction of tca
to oxidize AcoA to co2
form Nadh and Fadh2 for etc
synthesis of several other molecules for other pathways
each molecule of coA entering to tca yields:
2/3 co2
3 nadh
1 fadh2
1 gtp
name the molecules of the tca
"can i keep selling sex for money, officer?"
citrate
isocitrate
alpha keto glutarate
succinyl coA
succinate
fumarate
malate
OAA
pyruvate -> AcoA
pyruvate dehydrogenase
AcoA -> citrate
citrate synthase
citrate -> isocitrate
c. isomerase
isocitrate -> alpha keto glutarate
isocitrate dehydrogenase
alpha keto glutarate -> succinyl coA
alpha keto glutarate dehydrogenase
succinyl CoA -> succinate
thiokinase
succinate -> fumarate
succinate dehydrogenase
6 atp's that are needed to generate glucose from pyruvate
1. Ala carries amino groups to liver from muscle
2. oaa can replenish TCA or be used in gluconeogenesis
3. transition from glycolysis to tca cycle
4. end of anaerobic glycolysis
major ending pathway is pyruvate for these sites
rbc
leukocyte
kidney medulla
lens
testes
cornea
end of anaerobic glycolysis
pyruvate -> lactate or
pyruvate -> alanine
enzymes for 5 fates of pyruvate in cytosol
ldh, ALT. pyr decarboxylase
enzymes for 5 fates of pyruvate in mitochondria
PDH
PC
causes backup of pyruvate and alanine, resulting in lactic acidosis
pyruvate dehydrogenase deficiency
only a.a's that don't stimulate lactic acidosis
purely ketogenic a.a.'s - lys and leu
how one gets pyruvate dehydrogenase deficiency
congenital or
acquired - alcoholics due to b1 deficiency
findings of pyruvate dehydrogenase deficiency
neurologic defects
treatment of pyruvate dehydrogenase deficiency
high intake of ketogenic nutrients (high fat content or high lysine and leucine)
lactic acid buildup causes
stimulates GABA
denatures proteins
hyperkalemia
pyruvate dehydrogase complex catalyzes what reaction?
pyruvate -> AcoA
seen on lab of pyruvate dehydrogenase deficiency
high lactate/ high pyruvate levels
lactic acidosis
lactic acidosis + neurologic deficits (developmental delay, abnormal muscle tone, seizure)
pyruvate dehydrogenase deficiency
pyruvate dehydrogenase if rle for....
kreb cycle
location of TCA cycle
mitochondrial matrix
fuction of tca
to oxidize AcoA to co2
form Nadh and Fadh2 for etc
synthesis of several other molecules for other pathways
each molecule of coA entering to tca yields:
2/3 co2
3 nadh
1 fadh2
1 gtp
name the molecules of the tca
"can i keep selling sex for money, officer?"
citrate
isocitrate
alpha keto glutarate
succinyl coA
succinate
fumarate
malate
OAA
pyruvate -> AcoA
pyruvate dehydrogenase
AcoA -> citrate
citrate synthase
citrate -> isocitrate
c. isomerase
isocitrate -> alpha keto glutarate
isocitrate dehydrogenase
alpha keto glutarate -> succinyl coA
alpha keto glutarate dehydrogenase
succinyl CoA -> succinate
thiokinase
succinate -> fumarate
succinate dehydrogenase
isocitrate -> alpha keto glutarate
isocitrate dehydrogenase
alpha keto glutarate -> succinyl co a
alpha keto glutarate dehydrogenase
succinyl co a -> succinate
thiokinase
succinate -> fumarate
succinyl coA dehydrogenase
fumarate -> malate
fumarase
malate -> oaa
malate dehydrogenase
tca substrate for aa synthesis
alph keto glutarate
tca substrate for heme synthesis
succinyl coa
tca substrate for gluconeogenesis and fa synethesis
oaa
products of one turn of tca cycle
3 nadh
a fadh2
2/3 co2
1 gtp
sources of nadh in tca cycle
isocitrate -> alphketoglutarate
alpha keto glutarate -> succinyl coA
malate -> oaa
source of fadh in tca cycle
succinate -> fumarate
source of gtp in tca cycle
sunninyl co A -> succinate
allosteric inhibitors of citrate synthase
atp
nadph
succinyl coA
allosteric inhibitor of isocitrate dehydrogenase
atp
nadh
allosteric activator of isocitrate dehydrogenase
adp
allosteric inhibitor of alpha keto glutarate
succinyl coA
nadh
atp/gtp
1 round of tca yields this many atp
10 atp
1 glucose yields this many atp via tca alone
20 atp
2 pyruvate entering TCA yield this many atp
25 (+2 nadh)
1 glucose yields this many atp though tca and glycolysis
32 atp
glycolysis 5 atp from 2 nadh + 2 atp substrate phosphorylation
shuttles used to shuttle cytoplasmic NADH into mitochondria to etc
1. malate-asp shuttle
2. glycerophosphate shuttle
accepts e-s from NADH to become malate. malate can cross into mitochondria where it's oxidized to form NADH and OAA
malate-asp shuttle
dhap accepts ep's from NADH to become glycerophosphate. glycerophosphate enters mitochondria, where it's oxidized to form FADH2 and DHAP
glycerol-3-phosphate shuttle
accepts e-s from nadh in malate-asp shuttle to transfer across mitochondrial membrane
OAA
compound in malate-asp shuttle with ability to enter mitochondria
malate
in malate-asp shuttle, after malate enters mitochondria, is turned into this substance and gives off this
gives off NADH and forms into OAA
in malate-asp shuttle, OAA become.....at the mitochondria
aspartate, which may cross mitochondrial membrane back to the cytosol
no loss of atp with this napd shuttle
malate-asp shuttle
loss of atp with this nadh shuttle
glycerol-3-phosphate shuttle
nadh shuttle used only in need of rapid cell division
glycerol-3-phosphate shuttle
ages of rapid cell division
0-2
4-7
puberty
nadh transfers its e-s to this compound of the glycerol-3-ph shuttle
DHAP
DHAP becomes which substance that can cross mitochondrial membranes in glycerol-3-ph shuttle
g3p
compound in glycerol-3-ph shuttle with ability to enter mitochondria
g-3-p
in glycerol-3-ph shuttle what does g3p become and what does it give off?
gives off an fadh2 (instead of NADH) and becomes DHAP
net atp formed with malate-asp shuttle for 1 molecule glucose
32 atp
net atp formed with glyceraldehyde-3-ph shuttle for 1 molecule of glucose
30 atp
2.5 - 1.5 atp = 1 * 2 = 2 atp 32 - 2 atp = 30 atp
what molecules haveability to cross mitochondrial membranes in g3p shuttle?
g3p - into mitochondria
dhap - out of mitochondria
molecules that have ability to cross mitochondrial membrane in malate-asp shuttle?
malate -> into mitochondria
asp -> out of mitochondria
describe the malate asp shuttle
OAA accepts e-s from NADH to become malate. malate can enter mitochondria, where it's oxidized to NADH and OAA. OAA becomes asp and can exit mitochondria
describe the glycerol-3-ph shuttle
DHAP accepts e-s from NADH to become glycerophosphate. glycerophosphate enters mitochondria, where it's oxidized to form FADH2 and DHAP. dhap can exit the mitochondria to be used again
aa's that breakdown via pyruvate of tca
gly
ala
ser
aa's that breakdown via AcoA of tca
Lys
leu
phe
ile
thr
trp
aa's that breakdown via alpha keto glutarate of tca
glu
gln
aa's that breakdown via succinyl coA of tca
trp
tyr
phe
aa's that breakdown to OAA via tca
asp
asn
aa's that breakdown to fumarate via tca
proline
essential amino acids
"pvt tim hall"
phe
val
thr
trp
ile
met
his
arg
lys
leu
ketogenic aa
leu
lys
both glucogenic and ketogenic
phe
ile
trp
glucogenic aa's
val
thr
met
his
arg
acidic aa's
asp glu
basic aa's
arg
lys
his
most basic aa
arg
aa without charge at body ph
his
aa's required for periods of growth
arg
hi
aa's increased in hitones, that bind - charged dna
arg
lys
pathway that degrades amino acids into amino groups
urea cycle
accounts for 90% of N in urine
urea cycle
location of urea cycle
cytosol & mitochondria of hepatocytes
rate limiting step of urea cycle
carbamoyl phosphate synthase
urea cycle substrates
c02, nh3, asp,3 atp
products of urea cycle
urea, h2o, fumarate
allows for excretion by NH4+ by transferring ammonia into urea, which is excreted by kidneys
urea cycle
deficiency of urea cycle enzymes causes
hyperammonemia -> nh4+ intoxication and cns deterioration
name the components of the urea cycle
ornithine
carbamoyl phosphate
citrulline
aspartate
asparagine succinate
fumarate
arginine
urea
allosteric activator of carbamoyl phosphate synthase
n-acetyl glutamate
Vmax of carbamoyl phophate synthase
2 g/day
only step of urea cycle occuring in mitochondria
rate limiting step: co2 + nh4+ -> carbamoyl phophate via carbamoyl phosphate synthase