Exam 2 Flashcards
(114 cards)
1
Q
Catalyze or facilitate biochemical reactions
A
Enzymes
2
Q
If you __ enzyme activity, the likelihood of a reaction happening is ___
A
increase, increased
3
Q
If you __ enzyme activity, it will __ ATP production
A
lower, lower
4
Q
Are enzymes on and off switches or dimmer switches?
A
Dimmer switches
5
Q
Substrates bind to active site depending on shapes, like a puzzle
A
Key and lock concept
6
Q
If you have enough substrate, it will drive the reaction towards the products to try and reach equilibrium
A
Law of Mass Action
7
Q
They bind to sites on the enzyme away from the active site
A
Enzyme modulators
8
Q
Binding alters the enzyme’s function, either _____ or ______ activity at the active site
A
stimulating, inhibiting
9
Q
Modulation can occur through:
A
Electrochemical effects and conformational changes
10
Q
Electrochemical effects
A
Opposite charges attract > stimulating
Same charges repel > inhibiting
11
Q
Conformational changes
A
enzymes shapes alter affecting the active site’s function
12
Q
Who are the key allosteric modulators?
A
ATP and ADP
13
Q
Where are allosteric sites often located?
A
On backside of enzymes or non-catalytic regions
14
Q
Types of Enzyme Modulators
A
Minerals, B-vitamins, and high energy phosphates
15
Q
Minerals include:
A
magnesium, calcium, iron, and zinc
16
Q
B-vitamins include:
A
Niacin (NAD) and riboflavin (FAD)
Which are electron carriers to ETC
17
Q
High energy phosphates include:
A
ATP and ADP
18
Q
High energy state
A
ATP binds to enzymes (PFK) to inhibit further ATP production, showing energy supply is greater than demand
Potent inhibitor to prevent wasteful energy production
19
Q
Low energy state
A
ADP binds to enzymes to stimulate ATP production, showing energy demand is greater than supply
Potent activator to ramp up energy generation
20
Q
What is the ultimate goal of allosteric regulation?
A
Maintain energy balance:
ATP production = ATP demand with no excess accumulation of either
21
Q
Transfer phosphate molecules from one substrate to another
A
Kinase
22
Q
Adds free phosphate to substrate
A
Phosphorylase
23
Q
Removes phosphate from substrate and adds to free phosphate pool
A
Phosphatase
24
Q
Catalyzes anabolic reactions
A
Synthesase
25
Catalyzes oxidation or reduction reactions
Dehydrogenase
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Oxidation Process
Substrate Oxidation
Electron Carriers
Formation of NADH and FADH2
ETC
ATP Production
27
Substrate oxidation
Substrate loses electrons in pairs of hydrogen atoms
H2 - 2e- + 2H+
28
Electron Carriers (Oxidation)
NAD and FAD act as oxidizing agents and accept electrons and hydrogen atoms during oxidation
29
Formation of NADH and FADH2 (Oxidation)
NAD + 2e- + 2H+ - NADH + H
FAD + 2e- + 2H+ - FADH2
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ETC (Oxidation)
Electrons from NADH and FADH2 are transferred to ETC
Oxygen serves as the final electron acceptor
31
ATP Production (Oxidation)
The energy released during electron transfer is used to produce ATP through oxidative phosphorylation
32
Reduction Process
Substrate reduction
Reducing Agent
Formation of NAD
Cellular Processes
33
Substrate Reduction
Substrate gains electrons in pairs of hydrogen atoms
2e- + 2H+ - H2
34
Reducing Agent (Reduction)
NADH acts as a reducing agent by donating electrons to other molecules
Reduction occurs because adding electrons introduces a negative charge
35
Formation of NAD (Reduction)
NADH - NAD + 2e- + 2H+
36
Cellular Processes (Reduction)
Electrons are used in various biosynthetic reactions, including the Calvin cycle and other anabolic processes
37
Oxidation-Reduction Coupling
Electron transfer between molecules
Redox reaction explanation
Reverse reaction
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Electron transfer between molecules
In coupled reaction, one molecule is oxidized while another is reduced
A + NADH - A+ + NADH
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Redox reaction explanation
A undergoes oxidation (loses e-)
NAD undergoes reduction (gains e-)
A-H2 + NAD - A + NADH + H+
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Reverse reaction
NADH can donate electrons to another molecule, B, reducing it
NADH is oxidized back to NAD, and B is reduced to B-H2
NADH + B - NAD + B-H2
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Oxidation and Reduction
Oxidation - loses electrons
Reduction - gains electrons
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NAD/FAD are
electron carriers
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NADH is a
reducing agent
44
Oxygen is the
final electron receptor
45
The end product of redox reactions are
H2O and ATP
46
Redox coupling
one molecule is oxidized while another is reduced, allowing electron transfer through NAD and NADH
47
Immediate Energy System ATP ___ stored and PCr ____ stored
not truly, is
48
Immediate Energy System (Onset of Exercise)
Initial ATP Breakdown (energy release)
PCr System Activation
Sustained ATP Production
49
Initial ATP Breakdown (Onset of PCr)
Happens in the first seconds
ATPase facilitates this reaction
ATP + H2O - ADP +Pi + E
50
PCr System Activation (Onset of PCr)
PCr donates a phosphate group to ADP to regenerate ATP
Creatine kinase catalyzes this reaction
PCr + ADP - ATP +Cr
51
Sustained ATP Production (Onset)
After initial ATP and PCr stores deplete, other energy systems take over, but the PCr system remains crucial for short bursts of high-intensity effort
52
Immediate Post Exercise (Recovery)
Adenylate Kinase Reaction
Creatine Phosphate Regeneration
EPOC
53
Adenylate Kinase Reaction (Recovery)
During recovery, adenylate kinase helps regenerate ATP using two molecules of ADP
Adenylate kinase catalyzes this process
ADP + ADP - ATP + AMP
54
Creatine Phosphate Regeneration (Recovery)
Creatine combines with phosphate to reform PCr, allowing rapid ATP resynthesis for subsequent bouts of activity
Creatine kinase facilitates this reversible reactions
ATP +Cr - ADP + PCr
55
EPOC (Recovery)
After exercise, the body experiences EPOC to restore oxygen levels, replenish ATP and PCr stores and remove metabolic byproducts
56
Glycolysis:
breakdown of glucose
fast = non-oxidative (2 LA + 2 ATP)
slow = oxidative (2 pyruvate)
57
Glycogenolysis
breakdown of glycogen
fast = lactate + 3 ATP
slow = pyruvate - mitochondria = lots of ATP
58
Gluconeogenesis
synthesis of new glucose from non-CHO sources
metabolic acids, fats, protein
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Glycogenesis
synthesis of glycogen from glucose
60
Glycolysis starting molecule and ending molecule
Glucose to pyruvate
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Key substrates of glycolysis
Glucose, fructose, phosphoglycerate, glyceraldehyde, PEP, pyruvate
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Limiting steps of glycolysis
Hexokinase
PFK-1
Pyruvate Kinase
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Hexokinase (Glycolysis)
Catalyzes phosphorylation of glucose to glucose 6-phosphate using ATP
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PFK-1 (Glycolysis)
Catalyzes conversion of fructose 6-phosphate to fructose 1 and 6-biphosphate
Major rate limiting enzyme, highly regulated by ATP and AMP levels
65
Pyruvate Kinase
Catalyzes the final steps of glycolysis, converting PEP to pyruvate and generating ATP
66
ATP Cost vs ATP Produced (Glycolysis)
2 ATP used during initial phosphorylation steps (1 by hexokinase and PFK-1)
4 ATP produced later on (2 by pyruvate kinase and phosphoglycerate kinase)
Net Gain = 2 ATP
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NADH (Glycolysis)
2 are produced from oxidation by glyceraldehyde 3-phosphate dehydrogenase
Net Gain = 2
68
FADH2 (Glycolysis)
not directly produced in glycolysis, later on in the Krebs cycle
69
Number of Carbons: start vs finish
1 molecule of glucose = 6 carbons
vs
2 molecules of pyruvate = 6 carbons
70
What is the key factor of determination of speed for glycolysis?
Mitochondrial enzyme activity
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High mitochondrial enzyme activity
Pyruvate enters mitochondria for oxidative (slow) glycolysis
72
Low mitochondrial enzyme activity
Pyruvate is converted to lactate (fast glycolysis)
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Determinants of Mitochondrial Enzyme Activity
Oxygen availability (most important)
Mitochondrial temperature (hypothermia increases, hyperthermia decreases)
pH level (high acidity = lower enzyme efficiency)
74
Extracellular Lactate Shuttle
Transported nearby oxidative muscle fibers (Type 1)
Used by the heart (prefers lactate as fuel)
Delivered to distant muscle fibers for energy
75
Cori Cycle (gluconeogenesis in liver)
Converts lactate from muscle to pyruvate to glucose in the liver
Glucose gets sent back to muscle via blood
Occurs during recovery or low-intensity exercise
Involves oxidation (lactate to pyruvate) and reduction (pyruvate to lactate) reactions
76
Regulation of Glycolysis
Energy state of cell
Substrate/Product feedback
Acidity
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Energy state of cell (glycolysis)
High ADP = high demand for ATP which activates PFK
High ATP = low demand inhibits PFK
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Substrate/Product feedback (glycolysis)
Glucose > G-6-Phosphate activates hexokinase
Glucose < G-6-Phosphate inhibits hexokinase
79
Acidity (glycolysis)
Low pH inhibits key enzymes like PFK, slowing glycolysis
80
Glycogenolysis
breakdown of glycogen in muscle and liver
Main enzyme is glycogen phosphorylase (PHOS)
81
Muscle glycogen (glycogenolysis)
Primary fuel source for exercise lasting longer than 10 seconds
Skips glucose phosphorylation and produces 3 ATP per glucose
Occurs in skeletal muscle
Glycogen - Glucose-1-P - Pyruvate + 3 ATP + 2 NADH
82
Liver glycogen (glycogenolysis)
Maintains blood glucose levels during prolonged exercise
Contains G-6-Phosphatase to convert G-6-P to free glucose
Liver uses fatty acids for its own energy needs (does not rely on glycolysis)
83
Regulation of Glycogenolysis
Extrinsic regulation
Glucagon (pancreatic alpha cells) - stimulates liver glycogen breakdown
Activated during fasting or prolonged exercise to maintain blood glucose
84
What are the two defenses against hypoglycemia?
Glycogenolysis and Gluconeogenesis:
85
Glycogenolysis against hypoglycemia
using G-6-Phosphatase to release glucose from glycogen
86
Gluconeogenesis against hypoglycemia
creates new glucose from metabolic acids (LA and pyruvate by Cori cycle)
fats (glycerol)
amino acids (Alanine from alanine-glucose cycle)
87
Triglyceride Breakdown
Triglycerides - Glycerol + Free fatty acids
Alanine from muscle to liver to converted glucose
Alanine also acts as a carrier for N and C
88
Gluconeogenesis Regulation is controlled by the:
Hypothalamic-Pituitary-Adrenal Axis (HPA Axis)
89
Hypothalamus senses ____ and stimulates ____
low blood glucose
Pituitary gland for growth hormone
Adrenal gland for epi and cortisol
90
What also promotes glucose formation from the pancreas?
Glucagon
91
Tissue Specific Regulators (Gluconeogenesis)
Adipocyte Lipolysis (epi, glucagon, cortisol & GH)
Alanine mobilization (mainly cortisol with glucagon)
Lactate/Metabolic acids (epi & glucagon)
92
Aerobic activity & glycolytic adaptations
increase hexokinase activity and muscle glycogen stores
neutral levels of PFK, LDH, PHOS
93
Anaerobic activity & glycolytic adaptations
increase PFK activity, lactate tolerance, and muscle buffering
neutral levels of LDH and PHOS
94
Oxidative Phosphorylation Timeline
Slow glycolysis to pyruvate oxidation
Krebs cycle (citric acid cycle)
95
Slow glycolysis to pyruvate oxidation
Glycolysis ends with 2 pyruvate = 6 carbons
Each pyruvate - Acetyl-CoA (2 C) via PDH
Byproducts include 2 NADH, 2 CO2, and no ATP or FADH2
96
Krebs Cycle
Input 2 Acetyl-CoA (2 C each) with an end product of regeneration of oxaloacetate
Per Glucose Molecule (2 Cycles)
4 CO2, 2 ATP, 6 NADH, 2 FADH2
97
Total from pyruvate oxidation and Krebs cycle
8 NADH, 2 FADH2, 2 ATP, 6 CO2
98
Electron Transport Chain location and function
Inner mitochondrial membrane
Oxidizes NADH/FADH2 - generates ATP
99
ATP Yield of ETC
Each NADH = 3 ATP
Each FADH2 = 2 ATP
ATP "toll" = 1 ATP lost for shuttling NADH from glycolysis into mitochondria
100
Final ATP totals per glucose
Glycolysis = 4-6 ATP
Pyruvate oxidation = 6 ATP
Krebs cycle = 18 ATP + 4 ATP
101
Krebs Cycle Regulation
Redox potential (ratio of NADH:NAD+ in mitochondria)
Energy State
102
Redox potential Krebs cycle
High redox potential (High NADH) = Krebs slow
Low redox potential (High NAD+) = Krebs speeds up
103
Energy state Krebs cycle
High ATP = Krebs slow
High ADP = Krebs speeds up
104
Outer Membrane
Barrier for the mitochondrion
105
Intermembrane space
Site of proton accumulation during ETC
106
Inner membrane
Contains ETC and ATP synthase complexes
107
Cristae
Folded structures increasing surface area for ETC
108
Matrix
Location of Krebs cycle and pyruvate oxidation
109
F Complex
Enzyme that produces ATP using proton gradient
110
Final Glycolysis Inputs vs Outputs
Input = Glucose, 2 ATP
Output = 2 PA, 2 ATP, 2 NADH
111
Final Pyruvate Oxidation Inputs vs Outputs
Input = 2 PA
Output = 2 Acetyl-CoA, 2 NADH, 2 CO2
112
Final Krebs Cycle Inputs vs Outputs
Input = 2 Acetyl-CoA
Output = 2 ATP, 6 NADH, 2 FADH2, 4 CO2
113
Final ETC Inputs vs Outputs
Input = 10 NADH, 2 FADH2
Output = 34 ATP, regenerates NAD+/FAD
114
Total ATP Inputs vs Outputs
Input = glucose ~ 36-38
Output = glycogen ~ 37-39
