• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/107

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

107 Cards in this Set

  • Front
  • Back
which step of ATP has a large -delta H
the nucloephillic attack of phosphate of the pentacovalent intermediate
something that is reduced gets?
it gets a Hydrogen thereby becoming reduced
alanine gets deaminated to become?
the keto form of pyruvate
the amount of electrons emitted by..

Complex 1
Complex 2
Complex 3
Complex 4
1) 4
2) none
3) 4
4) 2
Amount of hydrogens to equal 1 ATP?
4
this is used in Complex 2 of OX PHOS
it is where Succinate turns into fumarate of calvin cycle and frees FADH2 to be used in that cycle
Which has more ATP, FADH2 of NADH and why?
NADH because FADH2 missed complex 1 and therefore loses the opportunity for 4 more electrons = 1 lessATP
what are the nucleotides in Complex 1
they are riboflavin derivatives with Iron-sulfur centers and are electron ACCEPTORS
(FMN and FAD)
this complex passes protons from ubiquinol to cytochrome C
Complex III
coenzyme Q
also called ubiquinone and it is embedded in the inner membrane and accepts electrons
type of cytochrom C that is an acceptor of electrons
Fe2
Type of cytochrome C that is a donater
Fe3+
the pumping of protons causes these two things which ensure that ATP will be synthesized
Chemical potential with a change in pH such that the inside of the matrix is ALKALINE

Change in electrical potential such that the Inside is NEGATIVE
This is used to regulate Ox Phos in the case of ischemia
IF1 inhibitor
how does brown fat generate heat?
it pumps protons out of the matrix and they com back in through thermogenin and release heat
where does cyanide bind in order to stop ox phos?
binds to iron in the the heme of complex 4
how to treat cyanide poisoning
inhale amyl nitrate or IV NaNO2 in order to convert oxyhemoglobin to methemoglobin and confuse the cyanide
how many ATP and NADH do you get from 1 molecule of glucose in glycolysis?
NET 4 ATP and 2 NADH. It USES up 2 ATP earlier
this is the first step in glycolysis and it allows glucose to not leave the cell (rev or irrev?)
hexokinase, irreversible and requires ATP.

Glucose - Glucose 6 phosphate
This is the rate limited step of glycolysis
phosphofructokinase

Uses ATP and magnesium and is irreversible

Fructose 6-phosphate - fructose 1,6 bisphosphate
step of glycolysis that produces 2 end products. which one is further used in glycolysis
Aldolase, reversible

Fruc-1,6,bisphos ---> dihydroxyacetone phosphate (Used for TG synthesis) + glyceraldehyde 3 phosphate (used in glycolysis)
converts dihydroxyacetong to glyceraldehyde 3 phosphate
triose phosphate isomerase
after the split in glycolysis, this is the next step
glyceraldehyde 3 phosphate DH
(SPITS OUT NADH). Needs NAD+ to work this reaction

Gly3P ---> 1,3-Bisphosphoglycerate
this is the first step in glycolysis and it allows glucose to not leave the cell (rev or irrev?)
hexokinase, irreversible and requires ATP.

Glucose - Glucose 6 phosphate
This is the rate limited step of glycolysis
phosphofructokinase

Uses ATP and magnesium and is irreversible

Fructose 6-phosphate - fructose 1,6 bisphosphate
step of glycolysis that produces 2 end products. which one is further used in glycolysis
Aldolase, reversible

Fruc-1,6,bisphos ---> dihydroxyacetone phosphate (Used for TG synthesis) + glyceraldehyde 3 phosphate (used in glycolysis)
converts dihydroxyacetong to glyceraldehyde 3 phosphate
triose phosphate isomerase
after the split in glycolysis, this is the next step
glyceraldehyde 3 phosphate DH
(SPITS OUT NADH). Needs NAD+ to work this reaction

Gly3P ---> 1,3-Bisphosphoglycerate
after the creation of the first NADH in glycolysis, this is the next step
phosphoglycerate Kinase - spits out 1 ATP and is REVERSIBLE

1,3 - Bisphophoglycerate --> 3-phosphoglycerate
converts phosphoenolpyruvate to pyruvate
pyruvate kinase, IRREVERSIBLE, spits out an ATP
starting products of glycolyssi
glucose, 2 ADP, 2 Pi, 2 NAd+
End products of glycolysis
2 pyruvate, 2 ATP, 2 H+, 2 NADH, 2 H20
2 ways of regenerating NAD+ to be used in glycolysis
1) mitochondria (aerobic)- Slow and does not help in spring plus it is hard to get NADH into the mitochondria

2) anareobic in cytosol - pyruvate turns into Lactic Acid. this lowers pH and inhibits the F1 ATPase
As pH lowers, what happens to glycolysis
it slows down, as is shown by the lactic acid cycle
inhibitors of PFK-1
ATP, Citrate (things that would show that you have enough energy)
amplifiers of PFK-1
AMP, ADP, fructose 2,6-bisphophate (gluconeogenis)
pentose phosphate pathway is important for what?
to create NADPH and to produce Ribose 5-phosphate needed for nucleotide biosynthesis
Two enzymes in pentose phosphate pathyway that create NADPH
1) glucose 6-phosphate DH
2) 6-phosphogluconate DH
the oxidized form of glutathione has?
the Sulfer groups are bound together

-S---S-
The reduced form of glutathione has
the Sulfer groups unattached and each with its own hydrogen

-SH HS-
H202 gets converted to safe H20 via?
glutathione peroxidase and its remnants needs NADPH to comeback to the form it can be used to do it again
non-oxidative steps of pentose phosphate pathway
series of steps in order to regenerate glucose-6-phosphate from ribose-5-phosphate. Just a bunch of Carbon switches
ocular abnormalities, ataxia, global confusion, alcohol abuse
wernike encephalopathy
fatigue, irratability, sleep problems, ab pain, anorexia
beri beri
neural symptoms in infancy, ataxia, seizure
Pyruvate DH complex deficiency

tests by elevated blood lactate and normal pyruvate/lactate ratio (both go up
this is used for citric acid cycle from glycoysis
pyruvate DH

converts pyruvate into Acetyl CoA and CO2
source of Acetyl-CoA energy
reactive thiol group and high acyl group transfer potential
coenzyme A has this vitamin in it
pantothenic Acid
5 coenzymes of Pyruvate DH
thiamine pyrophosphate, FAD, Coa-SH, NAD+, Lipoic Acid(electron and acyl carrier)

IRREVERSIBLE

Converts Pyruvate - Acetyl CoA
3 enzymes of PDH complex
1) pyruvate DH
2) Dihydrolipoyl transacetylase
3) Dihydrolipoyl reducatse
Pyruvate DH
first step of PDH complex. Attached TPP to pyruvate. Then transfers this acetyl group to lipoic acid
Dihydrolipoyl transacetylase
2nd step of PDH Complex. transfers the acetyl group to CoA-SH forming Acetyl-CoA
Dihydrolipoyl reductase
remakes the lipoic acid and making NADH in order to be used again
turns on PDC and its activators
means that you want MORE energy...pyruvate DH Phosphatase...uses H20

activators: Mg, Ca, Insulin
turns off PDC
you want LESS energy, pyruvate dehydrogenase kinase uses ATP
Inhibitors of pyruvate DH KINASE
this is what turns off PDC...inhibitors of this (net is to turn ON PDC)

Pyruvate, ADP, Ca, Mg, K
Activators of pyruvate DH Kinase
this is what turns off PDC...inhibitors of this (net is to keep PDC OFF)

Acetyl Coa, NADH
is there any increase of CA intermediates when you add acetyl CoA to the CA?
no
Amino acid equivalent of oxaloacetate
Aspartate
Amino Acid equivalent of a-ketogluterate
Glutamate
first step of CA
citrate synthase

converts Oxaloacetate and Acety CoA ----> citrate
citrate goes to
isocitrate via ACONITASE (has a cis intermediate)
and is reversible
isocitrate goes to
a-ketogluterate via isocitrate DH, and this causes a RELEASE of NADH
what does a-ketogluterate go to
goes to succinyl CoA via the a-ketogluterate DH complex which is similar to PDH complex. uses an CoA-SH and releases NADH and CO2
Succinyl CoA goes to
Succinate. via Succinyl-CoA synthetase. releases GTP and CoA-SH
Succinate goes to?
Fumarate via Succinate DH. this creates FADH2 and is used for the complex 2 of the ETC
Fumarate goes to?
malate via FUMARASE. this is reversible and uses aspartate as a nitrogen donor
from malate?
goes to OAA via Malate DH. This generates an NADH. It has a high delta G but occurs because OAA levels are soooo low
inhibitors and activators of first step of CA cycle
inhibitors - NADH, succinyl Coa, citrate, ATP

activators - ADP
inhibitors and activators of 3rd step of CA cycle
isocitrate to a-keto

inhibitors - ATP

Activators - Ca, ADP
inhibitors and activators of fourth step of CA cycle
from a-keto to succinyl-CoA

inhibitors - succinyl-CoA, NADH

activators - Ca
what are the two ways to recreate NAD+ used to make NADH in glycolysis
malate aspartate shuttle, and glycerol-3-phosphate shuttle
how do you creat NAD+ using the glycerol 3 phosphate shuttle?
you convert dihydroxyacetone phosphate into G3P thereby releaseing NAD+. then you use G3P and FAD to creat the dihydroxyacetone again
in order to be taken up in cells, what must TGs be hydrolyzed to and where?
to fatty acids and glycerol in the mitochondrial matrix
what is packaged into VLDL
FA from chylomicrons or FA in the liver
this hydrolyzes TGs to release the glycerol and FA
hormone-sensitive lipase
these regulate access to the lipids in adipocytes
perilipins
this induces the perilipins and needs the hormone-sensitive lipases to allow relase of FA in order to travel in blood via albumin
PKA from cAMP
how else can the kidney and liver make glycerol 3 phosphate?
can be formed by glyucerol and glycerol kinase
,pst pf the glycerol 3 phosphate comes from?
dihydroxyacetone
what 3 enzymes are needed to turn the dihydroxyacetone phosphate into a TG
1) Gly-3-phos DH (spits out NAD+) leads to Gly-3-p

2) acyl transferase makes it into phosphatidic acid

3) phosphatidic acid phosphatase and acyl transferase again make it a TG. or it can go and be a glycerolphospholid with a head group attachment
once the FA is in the adipose tissue, what is the first step of how does it get into the mitochondria?
1) it uses pyrophosphate and fatty acyl coA synthetase to be converted to fatty-acyl-Coa
what is teh second step fo FA getting into the mitochondria
it goes through carnitine acyltransferase 1 to get into intermembrane space, and then carnitine acyltransferase 2 to get into the mitochondria
what inhibits carnitine acyl transferase 1 thereby preventing fatty acid synthesis and degradation from occuring at the same time?
malonyl-CoA
first step in beta oxidation (FA breakdown)
pamitoyl-CoA gets turned into enoyl-CoA using a similar structure to succinate DH and it is called ACYL-CoA DH and makes FADH2
what does acyl CoA resemble?
it creats the FAD and goes straight to cytochrome Q thereby bypassing complex 1 making 6 protons instead of 4
in what step does water get added to the enoyl-CoA in B-oxidation
2nd step, using an enoyl-CoA hydratase to make L-B-hydroxyacyl-CoA
what does the L-B-hydroxyacyl-CoA get turned into
using B-hydroxyacyl-CoA DH and emitting NADH, it creats B-ketoacyl-Coa
last step of B-oxidation
B-ketoacyl-Coa gets made into 2 acetyl-CoA via acyl-CoA acetyltransferase (THIOLASE)
how do you do B-oxidation on a monounsaturated(double bond)
you need to move the double bond to make it trans via enoyl-CoA isomerase
what is the problem with an odd number FA
the last step produces 1 Acetyl coA and 1 propionyl CoA insteeaed of just 2 Acetyl-CoA
what do you do with a propionyl CoA
u turn it into an even number by using propionyl-CoA carboxylase and bicarb, ATP, and BIOTIN to creat D-methylmalonyl CoA
D-methylmalonyl CoA turns into L-methylmalonyl-CoA which then can turn into?
turns into succinyl CoA (used in CA cycle) via COENZYME B12!! and the use of methyl-malonyl-CoA mutase
amount of ATP generated by palmitoyl-CoA
108
what happens when you have EXCESS acetyl Coa?
it gets converted into Ketone bodies
first step of ketone acid synthesis
2 acetyl CoA come together via thiolase and make acetoacyl-CoA
2nd step in ketone acid synthesis
HMG coA synthase makes HMG-CoA with the use of acetoacylCoA and another Acetyl Coa
3rd step of ketone acid synthesis, to make acetoacetate
use HMG-CoA lyase to spit off one of the acetyl CoA from HMG-CoA to make acetoacetate
two products of acetoacetate and their importance
1) acetone via decarboxylase (bad)
2) d-B-hydroxybuterate which is ketone bodies and forms from D-B-HB DH and uses NADH
ketone bodies can not be used by what as fuel?
liver
ketone bodies cannot be used in the liver because it is missing this enzyme to break them down into their acetyl CoA derivatives1
B-ketoacyl-CoA transferase which converts acetoacetate into acetoacetyl-CoA while converting succinyl CoA into Succinate
____ and ___ combine to make
____ which combines with Acetyl CoA and makes _____ which leaves the mitochondria and reverse happens to get acetyl-CoA into cytosol so it can be used to make FA. what do u need to run all of this?
1) pyruvate & Malate

2) OAA

3) Citrate

need NADPH to run the entire thing
commited step of FA synthesis
acetyl-CoA carboxylase which combines acetyl coA and biotin in order to make malonyl CoA
malonyl CoA is attached to what to start FA synthesis?
acyl carrier protein domain of fatty acid synthase at the serine residue near the panthothenic acid
what happens first to malonyl CoA on the FA synthase
condensation and decarboxylation to add 2 carbon units
what happens 2nd to malonyl coA?
the B-keto product is reduced with the USE OF NADPH
what happens last to malonyl coA in FA synthase?
the acyl chain translocates to the cystein residue and the next malonyl coA can start all over again.