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323 Cards in this Set
- Front
- Back
|
complexes in etc
|
I
II CoQ = ubiquitin III IV V |
|
|
complex 1 aka
|
nadph dehydrogenase
|
|
|
complex 5 aka
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atp synthase
|
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location of etc
|
mitochondrial membrane
|
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e's from nadh and fadh2 are transferred to.....
|
ubiquitin
|
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complexes containing Fe
|
3 and 4
|
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atp synthase
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complex 5
|
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complex that needs cu
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4
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complexes containing heme groups
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3 and 4
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complexes with ability to pump H+'s to intramembranous space
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1
3 4 |
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complex which allows H+'s to be pumped across matrix
|
5
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how complex 5 creates ATP
|
uses gradient from H+; it has a proton channel that allows for protons to cross into matrix
|
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atp yielded by nadh
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2.5 atp
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atp yielded by fadh2
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1.5 atp
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how does complex 4 create h20
|
e-s are transferred to 02, which combine with h to form h2o
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ubiquitous: hexokinase or glucokinase
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herokinase
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found only at liver and pancreas: hexokinase or glucokinase
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glucokinase
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allosteric activator of glucokinase/hexokinase
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insulin
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allosteric inactivator of glucokinase/hexokinase
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glucagon
|
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high affinity: hexo or gluco kingase
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hexokinase (low km)
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low affinity: hexo or gluco kinase
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glucokinase (high km)
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high capacity: hexo or glucokinase
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glucokinase
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no feedback inhibition: gluco or hexokinase
|
glucokinase
|
|
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phosphorylates excess glucose after a meal to sequester at the liver
|
glucokinase
|
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energy source of brain: N, under stress, and under extreme stress
|
N - glucose
stress - glucose extreme stress - ketones |
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energy sources of heart
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N - FFA
stress - glucose extreme stress - glucose |
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energy sources of muscle
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N - glucose
stress - FFA extreme stress - FFA |
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energy sources of rbc
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N - glucose
stress - glucose extreme stress - glucose |
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always seen with disrupted glycolysis? and why?
|
hemolytic anemia bc glycolysis is the only source of energy for the rbc
|
|
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glucose -> g6p
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glucokinase (hexokinase)
|
|
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g6p -> f6p
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g6p isomerase
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f6p -> f1,6dp
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fructose 6 phosphate kinase = pfk1
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f6p -> f2,6dp
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f6p kinase
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f16dp splits into.....
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dhap and g3p
|
|
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cuts f16bp into 2 3 c molecules
|
aldolase a
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conversion bt dhap and g3p
|
triose phosphate isomerase
|
|
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g3p -> g1,3bp
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g3p dehydrogenase
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g1,3bp -> 3pg
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phosphoglycerate kinase
|
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3pg -> 2pg
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mutase
|
|
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2pg -> pep
|
enolase
|
|
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pep -> pyr
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pyruvate kinase
|
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pyruvate -> AcoA
|
pyruvate dehydrogenase
|
|
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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 |
|
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ATP synthase
|
complex V
|
|
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directly inhibit electron transport
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electron transport inhibitors
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|
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causes of low proton gradient and block of ATP synthesis
|
electron transport inhibitors
|
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directly inhibit mitochondrial APTase
|
ATPase inhibitors
|
|
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causes an increased proton gradient, but no ATP is produced because electron transport stops
|
atase inhibitors
|
|
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decreases permeability of membrane
|
uncoupling agent
|
|
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causes decreased proton gradient and how o2 consumption
|
uncoupling agents
|
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atp synthesis stops, but electron transport continues
|
uncoupling agents
|
|
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internal combustion
|
uncoupling agents
|
|
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inhibits complex I
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rotenone
amytal |
|
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inhibits complex II
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malonate
|
|
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inshibits complex III
|
antimycin
|
|
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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
|
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# of atp consumed in glycolysis
|
2 atp
|
|
|
rate limiting step of glycolysis
|
fructose 6 p -> fructose 1,6 bp via PFK1
|
|
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# 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 |
|
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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
|
|
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allosteric activator of PFK
|
fructose 2 6 biphosphate
insulin amp |
|
|
allosteric inhibitor of PFK
|
glucagon
atp citrate |
|
|
glycolytic enzyme deficiency causes....
|
hemolytic anemia
|
|
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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 |
|
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step of glycolysis that yields nad+
|
g3p -> g13dp via g3p dehydrogenase
|
|
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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
|
|
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F1,6BP -> F6P
|
fructose 1,6 bisphosphatase
|
|
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g6p -> glucose
|
glucose 6 phosphatase
|
|
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biotin and ATP requiring
|
pyruvate carboxylase
|
|
|
pyruvate carboxylase's allosteric activator
|
AcoA
|
|
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pyruvate carboxylase's allosteric inhibitor
|
glucose, adp
|
|
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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
|
|
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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
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"can i keep selling sex for money, officer?"
citrate isocitrate alpha keto glutarate succinyl coA succinate fumarate malate OAA |
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pyruvate -> AcoA
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pyruvate dehydrogenase
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AcoA -> citrate
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citrate synthase
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citrate -> isocitrate
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c. isomerase
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isocitrate -> alpha keto glutarate
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isocitrate dehydrogenase
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alpha keto glutarate -> succinyl coA
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alpha keto glutarate dehydrogenase
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succinyl CoA -> succinate
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thiokinase
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succinate -> fumarate
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succinate dehydrogenase
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isocitrate -> alpha keto glutarate
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isocitrate dehydrogenase
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alpha keto glutarate -> succinyl co a
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alpha keto glutarate dehydrogenase
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succinyl co a -> succinate
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thiokinase
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succinate -> fumarate
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succinyl coA dehydrogenase
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fumarate -> malate
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fumarase
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malate -> oaa
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malate dehydrogenase
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tca substrate for aa synthesis
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alph keto glutarate
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tca substrate for heme synthesis
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succinyl coa
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tca substrate for gluconeogenesis and fa synethesis
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oaa
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products of one turn of tca cycle
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3 nadh
a fadh2 2/3 co2 1 gtp |
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sources of nadh in tca cycle
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isocitrate -> alphketoglutarate
alpha keto glutarate -> succinyl coA malate -> oaa |
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source of fadh in tca cycle
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succinate -> fumarate
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source of gtp in tca cycle
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sunninyl co A -> succinate
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allosteric inhibitors of citrate synthase
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atp
nadph succinyl coA |
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allosteric inhibitor of isocitrate dehydrogenase
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atp
nadh |
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allosteric activator of isocitrate dehydrogenase
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adp
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allosteric inhibitor of alpha keto glutarate
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succinyl coA
nadh atp/gtp |
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1 round of tca yields this many atp
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10 atp
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1 glucose yields this many atp via tca alone
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20 atp
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2 pyruvate entering TCA yield this many atp
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25 (+2 nadh)
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1 glucose yields this many atp though tca and glycolysis
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32 atp
glycolysis 5 atp from 2 nadh + 2 atp substrate phosphorylation |
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shuttles used to shuttle cytoplasmic NADH into mitochondria to etc
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1. malate-asp shuttle
2. glycerophosphate shuttle |
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accepts e-s from NADH to become malate. malate can cross into mitochondria where it's oxidized to form NADH and OAA
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malate-asp shuttle
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dhap accepts ep's from NADH to become glycerophosphate. glycerophosphate enters mitochondria, where it's oxidized to form FADH2 and DHAP
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glycerol-3-phosphate shuttle
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accepts e-s from nadh in malate-asp shuttle to transfer across mitochondrial membrane
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OAA
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compound in malate-asp shuttle with ability to enter mitochondria
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malate
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in malate-asp shuttle, after malate enters mitochondria, is turned into this substance and gives off this
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gives off NADH and forms into OAA
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in malate-asp shuttle, OAA become.....at the mitochondria
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aspartate, which may cross mitochondrial membrane back to the cytosol
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no loss of atp with this napd shuttle
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malate-asp shuttle
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loss of atp with this nadh shuttle
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glycerol-3-phosphate shuttle
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nadh shuttle used only in need of rapid cell division
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glycerol-3-phosphate shuttle
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ages of rapid cell division
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0-2
4-7 puberty |
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nadh transfers its e-s to this compound of the glycerol-3-ph shuttle
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DHAP
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DHAP becomes which substance that can cross mitochondrial membranes in glycerol-3-ph shuttle
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g3p
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compound in glycerol-3-ph shuttle with ability to enter mitochondria
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g-3-p
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in glycerol-3-ph shuttle what does g3p become and what does it give off?
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gives off an fadh2 (instead of NADH) and becomes DHAP
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net atp formed with malate-asp shuttle for 1 molecule glucose
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32 atp
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net atp formed with glyceraldehyde-3-ph shuttle for 1 molecule of glucose
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30 atp
2.5 - 1.5 atp = 1 * 2 = 2 atp 32 - 2 atp = 30 atp |
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what molecules haveability to cross mitochondrial membranes in g3p shuttle?
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g3p - into mitochondria
dhap - out of mitochondria |
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molecules that have ability to cross mitochondrial membrane in malate-asp shuttle?
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malate -> into mitochondria
asp -> out of mitochondria |
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describe the malate asp shuttle
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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
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describe the glycerol-3-ph shuttle
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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
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aa's that breakdown via pyruvate of tca
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gly
ala ser |
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aa's that breakdown via AcoA of tca
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Lys
leu phe ile thr trp |
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aa's that breakdown via alpha keto glutarate of tca
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glu
gln |
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aa's that breakdown via succinyl coA of tca
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trp
tyr phe |
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aa's that breakdown to OAA via tca
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asp
asn |
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aa's that breakdown to fumarate via tca
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proline
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essential amino acids
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"pvt tim hall"
phe val thr trp ile met his arg lys leu |
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ketogenic aa
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leu
lys |
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both glucogenic and ketogenic
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phe
ile trp |
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glucogenic aa's
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val
thr met his arg |
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acidic aa's
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asp glu
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basic aa's
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arg
lys his |
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most basic aa
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arg
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aa without charge at body ph
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his
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aa's required for periods of growth
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arg
hi |
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aa's increased in hitones, that bind - charged dna
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arg
lys |
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pathway that degrades amino acids into amino groups
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urea cycle
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accounts for 90% of N in urine
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urea cycle
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location of urea cycle
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cytosol & mitochondria of hepatocytes
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rate limiting step of urea cycle
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carbamoyl phosphate synthase
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urea cycle substrates
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c02, nh3, asp,3 atp
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products of urea cycle
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urea, h2o, fumarate
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allows for excretion by NH4+ by transferring ammonia into urea, which is excreted by kidneys
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urea cycle
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deficiency of urea cycle enzymes causes
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hyperammonemia -> nh4+ intoxication and cns deterioration
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name the components of the urea cycle
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ornithine
carbamoyl phosphate citrulline aspartate asparagine succinate fumarate arginine urea |
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allosteric activator of carbamoyl phosphate synthase
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n-acetyl glutamate
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Vmax of carbamoyl phophate synthase
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2 g/day
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only step of urea cycle occuring in mitochondria
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rate limiting step: co2 + nh4+ -> carbamoyl phophate via carbamoyl phosphate synthase
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