Kin 17-Human Biochemistry-Final

Front 1

2 stages of the Krebs cycle?

Back 1

Stage 1: Oxidize Carbon atoms ot CO2

Stage 2: Regenerate Oxaloacetate

Front 2

At what points do we regulate the TCA?

Back 2

At the entry into the cycle-Acetyl CoA

Isocitrate dehydrogenase: stage between isocitrate and alpha-ketoglutarate

Alpha-ketoglutarate: stage between alpha-ketoglutarate to succinylcholine CoA

Front 3

Purpose of the Glyoxylate cycle?

Back 3

To convert fats to carbohydrates

Front 4

What happens in the cycle?

Back 4

Idocitrate is cleaved into succinate and glyoxylate.

Glyoxylate is converted to Malate which is reduced to Oxoaloacetate. Which restarts the cycle.

Front 5

What is the purpose of the ETC?

Back 5

Use high energy electrons to make ATP

Front 6

Where does it get its electrons from?

Back 6

NADH and FADH2

Front 7

What are the names of the complexes?

Back 7

C1: NADH- Q oxidoreductase

C2: Succinate- Q oxidoreductase

C3: Q-Cytochrome C Oxidoreducatse

C4: Cytochrome C Oxidase

Front 8

How many protons does NADH pump? and where?

Back 8

10 H+ in total.

C1: 4

C3: 4

C4: 2

Front 9

Where does FADH2 enter? Why?

Back 9

It enters at C2, which isn't actually a proton pump. It has lower reduction potential.

Front 10

Ultimate electron acceptor?

Back 10

OXYGEN

Front 11

What are the 2 gradients in the proton motive force?

Back 11

Chemical --> pH

Electrical --> Unequal distribution of protons

Front 12

ATP Synthase structure?

Back 12

2 parts

Fo = embedded in the inner mitochondria membrane

F1= In the matrix

Front 13

Characteristics of Fo

Back 13

2 half cylinders. One side open to the cytoplasm the other to the matrix.

2 helices span the middle with aspartic acid residue.

Protons flow through the cylinder and keep it rotating in one direction.

Front 14

Characteristics of F1

Back 14

3 Beta subunits

-Open, Loose (traps ADP and Pi) and Tight (synthesize ATP)

-3 alpha units divide the 3 betas

Front 15

What is the Y subunit?

Back 15

The subunit that connects the Fo and F1. It spins and interacts with the beta subunits. They DON'T move, but change shape.

Front 16

How many protons does it take to make 1 ATP

Back 16

3

Front 17

How many ATP are generated per NADH or per FADH2

Back 17

NADH = 2.5

FADH2= 1.5

Front 18

What is the process starting from Glucose?

Back 18

Glucose --> Glycolysis --> Pyruvate Dehydrogenase --> Citric Acid Cycle

Total = 30-32 ATP

Front 19

What is Glycogen?

Back 19

A highly branched polymer of Glucose. Held by alpha 1,4 glycosidic bonds.

Front 20

Where is it found?

WHY?

Back 20

Liver: to maintain blood-glucose levels

Muscle: Glucose needed for muscle contraction

Front 21

Key regulatory enzyme of Glycogen degradation?

What does it do?

Back 21

Glycogen Phosphorylase. It degrades glycogen from the non-reducing end.

Front 22

In what forms does it exist in?

Back 22

b-less active

a-more active

Each exists in a T and R state

Front 23

Muscle Glycogen Phosphorylase

Back 23

Default is b form in the T state.

However, it shifts to a form during muscle contraction.

Front 24

Liver Glycogen Phosphorylase

Back 24

Default is a form in the R state

It is always ready to make blood-glucose

Front 25

What does Insulin and Glucagon/Epinephrine do?

Back 25

Insulin deactivates. It dephosphorylates the serine residues

Glucagon/Epinephrine activates. It phosphorylates the serine residues

Front 26

Where is Glucagon found?

Back 26

in the LIVER ONLY

Front 27

Where is Epinephrine found?

Back 27

in BOTH the liver and muscle

Front 28

Define Glycogenin

Back 28

Glycogen priming enzyme. It makes alpha- 1,4 looks.

Front 29

Properties of glycogen synthase?

Back 29

Inactive when phosphorylated b form

Active when un-phosphorylated a form

Front 30

Purpose of the Pentose Phosphate Pathway

Back 30

Generating NADPH (reducing power) and pentose sugars

Front 31

What are the 2 phases?

Back 31

1. Making NADPH

2. Interconversion of sugars

Front 32

Stage 1?

Back 32

Glucose 6 phosphate converts itself. and pulls H+ and electrons generating the first NADPH

6-Phosphoglucono is converted into ribulose-5-phosphate and CO2. Generating the 2nd NADPH

Front 33

Stage 2?

Back 33

-Converting ribulose-5-P to RIBOSE-5-P. =adolase

-Converting ribulose-5-P to XYLULOSE-5-P. =ketolase

Front 34

What benefit do Transaldoses and Transketolases have?

Back 34

They can be used as substrates for many reactions. They link the PPP to glycolysis

Front 35

4 Modes?

Back 35

R-5-P > NADPH

R-5-P = NADPH

NADPH < R-5-P

NADPH & ATP needed

Front 36

Regulatory factor?

Back 36

The concentration of NADP+

Front 37

Erythrocytes?

Back 37

No nucleus, no synthesis and no need for pentoses.

HOWEVER they NO reducing power, because there's no mitochondria.

e.g. Red Blood Cells

Front 38

How is fat stored in adipose tissue?

Back 38

As traicylglycerols

Front 39

3 stages to degrade fat?

Back 39

1- Degrade the TAG into its fatty acids and glycerol into the blood.

2- F.A. must be activated and transported into the mitochondria

3-Degredation into acetyl CoA for processing in Krebs

Front 40

Name of the Fatty Acid Carrier?

Back 40

Serum Albumin

Front 41

Stage 1

Back 41

Activate the F.A.

It enters the cell and acetyl CoA attaches to it. Trapping it in the cell.

Front 42

Stage 2

Back 42

Acetyl CoA is exchanged for carnitine and translocated into the mitochondria.

Once inside, it returns to Acetyl CoA

Front 43

Stage 3-6

Back 43

Degradation- Known as Beta Oxidation

3-Oxidation

4-Hydration

5-Oxidation

6-Cleavage or 3 ketoacids.

Front 44

What's the equation used to find out how many Acetyl CoA's are needed?

To find out how many rounds of beta oxidation are required?

Back 44

n/2 = # of Acetyl CoA's

n/2 -1 = #rounds of beta oxidation

Front 45

How many ATPs does Palmitic Acid produce?

Back 45

106 ATP

Front 46

Ketone Bodies?

Back 46

Water soluble molecules produced during periods of starvation.

Front 47

Acetyl CoA vs. Ketone Bodies

Back 47

Acetyl CoA can't make glucose.

Ketone bodies can make glucose--they're a good glucose substitute.

Front 48

What does excessive ketone body accumulation result in?

Back 48

It causes acidosis which can lead to coma and death

Front 49

What is Acetyl CoA the end product of? and what is it the precursor for?

Back 49

Its the end product of Fatty Acid degradation and the precursor for all Fatty Acids.

Front 50

3 Stages to make fat?

Back 50

1- Move the Acetyl CoA from the mitochondria to the cytoplasm.

2- Start synthesis by activating Acetyl CoA to Malonyl CoA

3-Repeat addition/reduction of 2C until C16 is synthesized.

Front 51

Step 1?

Back 51

Getting out of the mitochondria

Acetyl CoA + oxaloacetate to make citrate.

Citrate can diffuse across the membrane.

Once in the cytoplasm it is cleaved back into acetyl CoA and oxaloacetate.

Front 52

Step 2?

important?

Back 52

Activating Acetyl CoA

It is carboxylated by Acetyl CoA Carboxylase

THIS IS THE COMMITTED STEP

Front 53

Step 3?

Back 53

Repitition of Addition/Reduciton of 2C units

by the FAS enzyme complex

Front 54

Characteristics of the FAS

Back 54

It is a dimer of 2 identical chains which has 2 active sites.

It also has 2 enzymatic compartments

1-Selection/Condensing: binds 2C and condenses them.

2- Modification: reduces and dehydrates

Front 55

FAS Reactions?

what does it start/end with?

Back 55

Acetyl ACP + Malonyl ACP

-Condensation

-Reduction

-Dehydration

-Reduction

=Butyryl ACP

Front 56

Essential Fatty Acids?

Back 56

18: 2n-6 --> inflmmatory

18: 3n-3 --> non-inflammatory

Front 57

Beyond 16C?

Desaturating?

Back 57

Elongation beyond 16C is done on the endoplasmic reticulum.

Elongases add 2C by Malonyl CoA

-Desaturation is done by Fatty Acid Desaturases, done from the carboy end

Front 58

Eicosanoids?

Back 58

Powerful hormones that are responsible for the beneficial effects of good fatty acids.

Front 59

Glucagon/Epinephrine vs. Insulin

Back 59

Glucagon/Epinephrine mobilizes fats and moves them into the blood to be used as fuel.

Insulin activates the Acetyl CoA carboxylase. It stimulates synthesis

Front 60

Precursor for triaclyglycerol and phospholipid synthesis

Back 60

Phosphatidate

Front 61

Main sites of synthesis

Back 61

Liver = triacylglycerol synthesis

ER = Phospholipid synthesis

Front 62

What does Phospholipid Synthesis require?

Back 62

An activated substrate.

Front 63

Steps?

Back 63

Activation of phosphatidate. Use CTP to create a diacylglycerol-CDP. the Alcohol can be swapped in.

OR

Activation of Alcohol group. Use CTP to create an intermediate. the Diacylglycerol can be swapped in.

Front 64

Where does Cholesterol synthesis occur?

Back 64

In the Liver

Front 65

Step 1?

Back 65

Isopentyl Pyrophosphate is synthesized.

3Acetyl CoA = HMG CoA reduced to Mevalonate (6C) (by HMG CoA reductase) COMMITTED STEP

Front 66

Step 2?

Back 66

Condensing 6 Isopentyl Pyrophosphate to form Squalene.

Front 67

Step 3?

Back 67

Squalene cyclizes and condenses to Cholesterol.

Lanosterol is formed and is then metabolized to cholesterol.

Front 68

How to regulate Cholesterol Synthesis

Back 68

Control HMG CoA in 4 ways

1. Synthesis of the mRNA

2. Translation into the active protein.

3. Activate enzymes that degrade it. by increased [cholesterol]

4. Phosphorylation of the reductase inactivates it. by AMP dependent-kinase

Front 69

Composition of Fatty Acids

Back 69

-Unestered cholesterol

-Cholesterol ester

-Phospholipid

-Apoprotein

Front 70

Lipoproteins?

How are they classified

Back 70

A group of soluble proteins that combine with fat or other lipids in the blood stream.

They are classified by density. The most lipid composition the least dense.

Front 71

Chylomicrons

LDL

HDL

Back 71

Chylomicrons= Biggest in diameter, most lipid = least dense

LDL= main carrier of cholesterol in the blood

HDL- Reverse Cholesterol transport. It carries the cholesterol released into the blood back to the liver.

Front 72

Purpose of the Urea cycle?

Back 72

To excrete ammonia. Some organisms can get rid of it, so it must be converted to urea to get rid of it.

Front 73

Steps of the Urea Cycle

Back 73

1. Couple Ammonia + Bicarbonate = Carbamoyl P. THE COMMITTED STEP

2. The Carbamoyl is transferred to Omithine= Citrulline

3. Citrulline condenses with Arginine= Argininosuccinate

4. Argininosuccinate is cleaved in Arginine and Fumarate

5. Arginine is cleaved into Urea and excreted.

Front 74

Fate of the Carbons?

Back 74

The are metabolized into 7 major metabolic intermediates.

-Ketogenic amino acids = can form fat. (CoA)

LEUCINE AND LYSINE ONLY

-Glucogenic amino acids = can make glucose

-Or they're ketogenic or glycogenic which are amino acids that yield products that can become glucose

Front 75

2 ways nucleotides are metabolized?

Back 75

De Novo=new

Salvage= Reusing an existing one.

Front 76

PRPP?

Back 76

It is the key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.

Front 77

UMP--> UDP-->UTP

Back 77

First = UMP specific nucleoside monophosphate kinases.

Second= Non-specific nucleoside diphosphate kinases.

Front 78

UTP --> CTP

UTP --> TTP

Back 78

Add an Amine group

Add a Methyl group

Front 79

Dihydrofolate Reductase

Back 79

An enzyme that reduces dihydrofolic acid to tetrahydrofolic acid, using NADPH as electron donor

Front 80

4 ways to fit DNA in a cell

Back 80

1. Supercoiling

2. Nucleosomes

3. Chromatin

4. Chromosomes