Biochem Flashcards
bond - sucrose
alpha 1, beta 2
bond - lactose
beta 1,4
bond - trehalose
alpha 1,1
bond - maltose
alpha 1,4
bond - isomaltose
alpha 1,6
reducing sugars
lactose, isomaltose, glucose, galactose
non-reducing sugars
sucrose, trehalose, raffinose
amylase breaks bonds?
alpha 1,4
isomaltase only one to break bonds?
alpha 1,6
results digestion alpha-amylase
40% maltose
30% alpha-dextrins
25% maltotriose
5% glucose OGS
membrane-bound complexes
sucrase isomaltase complex (jejunum) glucoamylase complex (ilem)
enantiomer
D and L glucose (mirror)
epimer
glucose and galactose
anomer
alpha and beta glucose
2 enzymes both cytoplasm and mitochondria
malate dehydrogenase
aspartate transaminase
and glycerol-3-P dehydrogenase too?
(shuttle)
3 controlling steps of glycolysis
- glucokinase/hexokinase
- PFK1
- pyruvate kinase
hexokinase vs. glucokinase
hexokinase = muscle and brain
non inducible, sensitive to cell’s needs, works best at low concentrations, inhibited by products (G6P), works with other sugars
glucokinase = liver, very sensitive to dietary glucose, works very quickly, inducible by insulin, only with glucose
PFK1 importance?
sensitive to energy charge of the cell
activated by fructose 2,6-bisphosphate and high AMP
inhibited by high ATP
first irreversible step unique glycolytic pathway
PFK1
mannose
importance for synthesis of glycoproteins
can be made from glucose
no enzyme to convert mannose6-P since mannose itself not needed
hexokinase can convert mannose 6-P into fructose 6-P, then fit in the glycolytic pathway
what enzyme does fructose bypass
PFK1
fructose metabolism
only in liver
converted to fructose 1-P and directly converted with aldolase to dihydroxyacetoneP and glyceraldehyde
this glyceraldehyde is not trapped and need to be phosphorylated to glyceraldehyde3P
insulin not required
easier to make pyruvate from fructose rather than convert to glucose
galactose conversion to glucose
not so easy, but primordial (infants)
trapped in the cell using galactokinase
galactose 1-P uridyltransferase does 2 things
1. take UMP from UDP to form glucose 1-P (de energizing)
2. adding this UMP and add it to galactose 1-P (energizing)
interconversion of galactose 1-P into glucose 1-P only possible when?
molecules energized
non classical galactosemia
lack which enzyme?
galactokinase (can’t trap galactose)
non classical galactosemia
symptoms?
diarrhea, vomiting, dehydration, cataracts
galactosemia and galactosuria
with galactosemia, cataracts due to?
aldose reductase converting galactose into galactitol, makes the lense of the eyes cloudy
classical galactosemia
lack of which enzyme(s)?
galactose 1-P uridyltransferase (can’t get rid of trapped galactose)
classical galactosemia
symptoms
diarrhea, vomiting, dehydration, cataracts, LIVER FAILURE + MENTAL RETARDATION
(galactosemia and galactosuria)
pyruvate dehydrogenase
mitochondria
3 enzymatic reactions
irreversible
coenzymes require thiamin, lipolic acid, riboflavine (FAD), niacin (NAD)
pyruvate dehydrogenase
3 controls
- direct inhibition by product (NADH and acetyl CoA)
2 and 3. covalent modification
inhibited by pyruvate dehydrogenase kinase (add a phosphate) when ATP, NADH and acetyl-CoA levels raise (no energy needed) and activated by pyruvate dehydrogenase phosphatase (remove the P) when pyruvate and Ca levels raise
GLYCOLYSIS
glucose
glucose ——-> glucose-6-P
(uses 1 ATP)
(glucokinase/hexokinase)
GLYCOLYSIS
glucose-6-P
glucose6P fructose6P
(phosphohexose isomerase)
GLYCOLYSIS
fructose-6P
fructose6P ——-> fructose 1,6-bisphosphate
(uses 1 ATP)
(PFK1)
GLYCOLYSIS
fructose 1,6, bisphosphate
fructose 1,6 bisP dihydroxyacetoneP + glyceraldehyde3P (aldolase)
GLYCOLYSIS
dihydroxyacetoneP glyceraldehyde3P
triosephosphate isomerase
GLYCOLYSIS
glyceraldehyde 3P
glyceraldehyde-3P 1,3-bisPglycerate
(glyceraldehyde3P dehydrogenase complex)
(produces 1 NADH/pyruvate)
GLYCOLYSIS
1,3-bisPglycerate
1,3bisPglycerate 3Pglycerate
(phosphoglycerate kinase)
(produces 1 ATP / pyruvate)
GLYCOLYSIS
3-Pglycerate
3Pglycerate 2Pglycerate
(phosphoglycerate mutase)
GLYCOLYSIS
2-Pglycerate
2Pglycerate phosphoenolpyruvate
(enolase)
GLYCOLYSIS
Penolpyruvate
Penolpyurvate —–> pyruvate
(produces 1 ATP/pyruvate)
(pyruvate kinase)
GLYCOLYSIS
Pyruvate
pyruvate lactate
(lactate dehydrogenase)
(recyles NADH + H+ into NAD+)
GLYCOLYSIS
3 controlling steps
- glucokinase/ hexokinase
- PFK1
- pyruvate kinase
oxaloacetate = catalytic or stochiometric?
catalytic, used over and over again
acetyl-CoA = catalytic or stochiometric?
stochiometric = substrate
oxaloacetate can be made from?
pyruvate —-> oxaloacetate
(pyruvate carboxylase)
(uses 1 ATP)
KREBS CYCLE
first step
acetyl-CoA + oxaloacetate —–> citrate
(citrate synthase)
KREBS CYCLE
citrate
citrate isocitrate
(aconitase)
KREBS CYCLE
isocitrate
isocitrate alpha-ketoglutarate (isocitrate dehydrogenase)
produces 1 NADH
KREBS CYCLE
alpha-ketoglutarate
alpha-ketoglutarate —–> succinyl-CoA
(alpha-ketoglutarate dehydrogenase complex)
(produces 1 NADH)
KREBS CYCLE
succinyl-CoA
succinyl-CoA succinate
(succinyl thiokinase)
(produces 1 ATP)
KREBS CYCLE
succinate
succinate fumarate
(succinate dehydrogenase)
(produces 1 FADH)
KREBS CYCLE
fumarate
fumarate malate
(fumarase)
KREBS CYCLE
malate
malate oxaloacetate
(malate dehydrogenase)
(produces 1 NADH)
KREBS CYCLE
3 controlling steps?
- citrate synthase
- isocitrate dehydrogenase (irreversible, 1st commited step of Krebs cycle)
- alpha-ketoglutarate dehydrogenase
energy production GLYCOLYSIS
glucokinase -1 ATP
PFK1 -1 ATP
glyceraldehyde 3-P dehy 1 NADH x2
phosphoglycerate kinase 1 ATP x2
pyruvate kinase 1 ATP X2
energy production KREBS
pyruvate dehydrogenase 1 NADH x2
isocitrate dehydrogenase 1 NADH x2
alpha-ketoglutarate dehydro 1 NADH x2
succinate thiokinase 1 ATP x 2
succinate dehydrogenase 1FADH X2
malate dehydrogenase 1 NADH x2
malonate
poison binds to active site of succinate dehydrogenase and stops the reaction, making Krebs linear and oxaloacetate stoiciometric
amphibolic
Krebs cycel can be used anabolically to form amino acid and glucose
and catabolically to produce energy from glucose
fluoroacetate
poison = fluorocitrate (similar enough to acetate) binds tightly to aconitase and disables it = stops the Krebs
ETS (Mitchell’s chemiosmotic theory)
outward pumping of hydrogen ions from mitochondrial matrix
oxidation of NADH and FADH2 in mitochondria by ETS
series of oxidized and reduced steps
ATPase is the only way to pump hydrogen ions back in
3 complexes (coQ10, iron, oxygen)
ETS - cyanide
blocks complex IV
ETS - barbital
blocks complex I (protons not pumped out, ATPase stops working)
ETS - antimycin A
blocks complex II
ETS - oligomycin
blocks ATPase
ETS - atratyloside
blocks adamine nucleotide transmutase (transport ADP inside and ATP outside)
Name 2 shuttles
glycerophosphate shuttle = 3 ATP
malate aspartate shuttle = 2 ATP
pentose shunt - 3 roles?
- used to produce NADPH (requires for fatty acid synthesis, cytochrome P450 detox, cholesterol synthesis)
- gives 5-carbon sugar (ribulose/ribose)
- converts 5-carbon sugar into glycolytic intermediates
important to provide nucleotide for protein synthesis
pentose shunt - oxidative part
oxidative = irreversible, very sensitive to NADPH levels, only run if needed
glucose-6P + 2 NADP+ —-> ribulose -5P + NADPH + 2 H+
pentose shunt - non-oxidative part
reversible
2 roles: produces ribulose5P when needed
can work reverse
ribulose-5P + ribose5P furctose 6P + glyceraldehyde3P
what happens to Krebs, ATPase and ETS if adequate ATP?
adequate energy
inhibit Krebs and slows down ETS
citrate synthase and isocitrate dehydrogenase are inhibited by ATP
if ATP is high, hydrogen ions build up outside mitochondria and ETS shut down
ATPase also inhibited by adequate ATP
Krebs, ETS and ATP levels are closely interrelated
If adequate ATP, extra glucose = glycogenesis and fatty acid synthesis
what happens to Krebs, ATPase and ETS if dinitrophenol (uncoupler)?
makes system less efficient
carries hydrogen inside mitochondria bypassing ATPase, making ETS increase its activity to try to pump H+ out, speeding up the Krebs cycle at the same time
= more fuel oxidation without generating ATP
= weight loss
generates a lot of heat, can be problematic for homeostasis and can also damage the liver (responsible for processing dinitrophenol)
if cyanidine
shuts down ETS, no reduced cofactors made, no proton gradient
reversible enzyme (enolase) controlled by?
substrate/ product
2 shuttle systems
glycerophosphate shuttle = 1 FAD
aspartate malate shuttle = 1 NAD
