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molecular processes Flashcards

1
Q

Summarise the five main functions of the Krebs cycle.

A
  • metabolic engine
  • oxidation of Acetyl-coA
  • CO₂ emission
  • reducing equivalent production (i.e. NADH and FADH₂)
  • GTP production

(approx. 10 ATP/cycle produced)

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2
Q

State the reducing equivalents and how they react in the Krebs cycle.

A
  • NAD⁺ reduction as it loses a hydride (H-) ion and a proton (H⁺): NAD⁺ → NADH + H⁺
  • FAD⁺ undergoes sequential reduction by hydrogen addition: FAD⁺ + H⁺ → FADH + H⁺ → FADH₂
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3
Q

Describe how enzymes of the Krebs cycle are named.

A
  • oxidoreductase → oxidation reactions to produce NADH and FADH₂
  • dehydrogenases → reactions involve loss of hydrogen (H)
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4
Q

Describe reaction 1 of the Krebs cycle.

Hint - Owen and Chris 2- the enzyme synthesizes this product

A
  • favourable under standard conditions
  • reaction driven by formation of citryl-coA intermediate which undergoes rapid hydrolysis
  • oxaloacetate + acetyl CoA → citrate (citrate synthase)
  • alongside: H₂O → CoA

(draw out using notes)

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5
Q

Describe reaction 2 of the Krebs cycle (2-step isomerisation).

(Hint - Can’t Carry It 2)

A
  • step 1: citrate -H₂O → cis-acotinate/intermediate (aconintase)
  • step 2: cis-acotinate/intermediate +H₂O → isocitrate (aconintase)
  • coordination of OH group in step 1
  • facilitation of rehydration in step 2 by active site 4Fe-4S cluster
  • mitochondrial form of aconitase enzyme used
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6
Q

Describe reaction 3 of the Krebs cycle (2-step decarboxylation and formation of NADH).

(Hint - India Owns A 3)

A
  • step 1: oxidation:
    isocitrate → (isocitrate dehydrogenase) oxalosuccinate intermediate
  • Step 2: decarboxylation
    oxalosuccinate intermediate → (isocitrate dehydrogenase) α-ketoglutarate
  • isocitrate dehydrogenase tightly-regulated
  • metabolic nodal point – other pathways produce α-ketoglutarate
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7
Q

Describe reaction 4 of the Krebs cycle (oxidative decarboxylation with NADH formation)

(Hint - Andy 1-2-3 Splat 4)

A
  • enzymatic mechanism with 3 subunits which catalyse different stages of reaction
  • α-ketoglutarate → [E1 +TPP (+ ↪CO₂) → E2 + lipoamide (+ ↪CoA) → E3 + FAD⁺ (+ ↪ NAD⁺ → NADH + H⁺)] aka the α-ketoglutarate dehydrogenase complex (intermediate) → succinyl CoA
  • note 1. is decarboxylation and 3. is oxidation of lipoamide

(see notes for details)

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8
Q

Describe reaction 5 of the Krebs cycle (substrate-phosphorylation).

(Hint - Sally Surfs 5)

A
  • succinyl-CoA → Succinate (succinyl-CoA synthase)
  • alongside: GDP + ADP → (nuceloside diphosphate kinase) GTP + ATP
  • enters E.T.C
    (phosphoryl transfer)
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9
Q

Describe reaction 6 of the Krebs cycle (reduction)

Hint - Sianise Flies 6

A
  • succinate → (succinate dehydrogenase) fumarate
  • alongside reduction: FAD → FADH₂
  • FADH₂ enters E.T.C via reduction of coenzyme Q10 in inner membrane of mitochondria
  • succinate dehydrogenase associated with membrane, and covalently-linked to FADH₂ molecule
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10
Q

Describe reaction 7 of the Krebs cycle (hydration)

Hint - Freya Can’t Match 7

A
  • fumarate → (fumarase + OH-) carboanion intermediate (fumarase + H⁺) → malate
  • hydration of C=C catalysed by stereospecific enzyme
  • formation of L-isomer of malate which is important for metabolite transporters across mitochondrial membranes
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11
Q

Describe reaction 8 of the Krebs cycle (oxidation)

Hint - Marley Owns 8

A
  • malate → oxaloacetate (malate dehydrogenase)
  • alongside: NAD⁺ → NADH + H⁺ (reduction)
  • oxidation of OH group regenerates oxaloacetate
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12
Q

How is the Krebs/Citric acid cycle studied and what happens to the carbons from acetyl CoA and how are some carbons lost?

A
  • carbons from Acetyl-coA are not ones lost via decarboxylation reactions
  • acetyl-coA carbons become incorporated into oxaloacetate at the end of the cycle
  • thus lost as CO₂ in subsequent turns of cycle
  • explored using 14C-labelling experiments

(see notes for summary drawing of cycle)

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13
Q

What drives the Krebs cycle?

Hint - to do with ΔG and certain steps

A
  • ΔG difficult to determine as in mitochondria and isolating w/o contaminating with cytosol difficult
  • steps 1, 3 and 4 → key regulatory points
  • step 8 not spontaneous with low oxaloacetate concentrations → can drive reaction forward
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14
Q

Name five enzymes which are key in regulating the Krebs cycle.

(Hint - PICAP - 1x creation, 3x remove H, remove CO₂ - α)

A
  • citrate synthase
  • isocitrate dehydrogenase
  • α-ketoglutarate dehydrogenase
  • pyruvate dehydrogenase
  • pyruvate decarboxylase
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15
Q

Describe oxidative phosphorylation in mitochondria.

A
  • 4 enzymes complexes (lots of proteins in them) embedded in membrane
  • NADH as e- donor passes through complex 1 (ubiquinone/nol) and 4 H⁺ pass through
  • with FADH₂ less ⁺ pumped → less ATP synthesis
    • QH is shuttle molecule
    • terminal complex so oxygen reduced to water

(see notes for diagrams)

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16
Q

What is reduction potential and what does it mean?

A
  • tendency of a species to accept electrons/become reduced
  • more positive the value the more likely to accept electrons
  • relative to a proton
  • biochemical standard reduction potential (E°’) is for a compound under standard conditions (like G°’)
  • as you go along ETC reduction potential of substrates increases
  • O₂ + 2H⁺ + 2e- → H₂O
17
Q

What is the general formula of saturated fatty acids?

A
  • CH₃(CH₂)nCOOH

- contain HC chain, terminal carboxylic acid group and cis or trans bonds

18
Q

Give 4 examples of saturated fatty acids.

A
  • stearic acid; octadecanoic acid, 1st C=C at C1, 18 Cs
  • oleic acid; ω 9-fatty acid, 1st C=C at C9, 18 Cs
  • linoleic acid; ω 6-fatty acid, 1st C=C at C6, 18 Cs
  • α-linoleic acid; ω 3-fatty acid 1st C=C at C3, 10 Cs

(see notes for details)

19
Q

Describe triacylglycerol metabolism.

A
  • glucose can be converted into fatty acyl glycerol
  • hormone-sensitive lipase used to conjugate fats to lipids and then transport fats
  • intracellular (unlike from lipoprotein + pancreatic lipase)
  • TAG → DAG → MAG → FFA + glycerol
TAG = triacyl glycerol
DAG = diacyl glycerol
MAG = monoacyl glycerol
FFA = free fatty acid
20
Q

What do high glucose levels cause for hormone-sensitive lipase?

A
  • inhibition of lipolysis (fat breakdown)
  • provides glycerol-3-phosphate from glycolysis
  • thus, promotes fat storage
21
Q

What are the 4 main roles of fatty acids?

Hint - Faisah Served Colourful Halvah

A
  1. fuel molecules – mostly stored in adipose tissue as triacylglycerols (i.e. triacylglycerol metabolism)
  2. structural – component of lipid membranes as attached to groups
  3. covalent modifications of proteins (dynamic and reversible)
    - increase interaction w/ membranes (lipid anchors)
    - promote protein-protein interactions
  4. production of fatty acid hormones - i.e. prostaglandins stimulate inflammation, modulate synaptic transmission, stimulate sleep
22
Q

Why is fatty acid synthesis regulated?

A
  • so catabolism (mitochondria) and anabolism (cytoplasm) don’t simultaneously occur (pathways not simply reversals of one another)
23
Q

What is stage 1 of fatty acid synthesis?

Hint - AM and lots of other molecules involved

A
  • acetyl CoA → (acetyl CoA carboxylase, ACC) malonyl CoA
  • alongside: HCO₃- + ATP → ADP + Pi
  • first step, irreversible, rate-limiting, allosteric enzyme
  • requires biotin (vitamin B7) and ATP

(see notes for details)

24
Q

What is stage 2 of fatty acid synthesis?

Hint - CoACP

A

1) acetyl CoA → acetyl ACP (acetyl trancylase)
- alongside: ACP → CoA
2) malonyl CoA → malonylACp (malonyl transacylase)
- alongside: (another) ACP → CoA
- ACP is a transport protein which binds to acetyl

25
Q

What are the final stages of fatty acid synthesis?

A

elongation steps:

  • feedback into addition of 2C from condensation w/ malonyl-ACP
  • condensation, reduction, dehydration, reduction…

(see notes for diagram)

26
Q

Describe acetyl-coA availability for fatty acid synthesis.

A
  • shuttle pathway used to move acetyl CoA from mitochondria to cytosol
  • NADPH produced and used
27
Q

Describe regulation of acetyl Co-A carboxylase (ACC) activity by insulin and glucagon.

(Hint - all things CIG)

A
  • citrate used to partially switch on fat breakdown pathway (partially actives carboxylase)
  • allosteric (citrate) and hormonal (insulin + glucagon) regulation of lipolysis
  • insulin → activates ACC
  • glucagon → deactivates ACC

(see notes for diagram)

28
Q

Describe fatty acid oxidation (activation).

Hint - +A or -P

A
  • adenosine added to activate fatty acyl-CoA
  • molecule then sent into mitochondria
  • pyrophosphate + fatty acyl-adenylate → fatty acid
  • removal of pyrophosphate helps thermodynamically drive reaction forward
29
Q

Why is beta-oxidation needed and what type of process is it?

A
  • to transport activated fatty acids across membranes
  • (inner fatty acids more impermeable to membrane)
  • a mitochondrial process
30
Q

State the 4 stages of beta-oxidation.

Hint - IHOT

A
  1. intro of a trans C=C bond between α and β Cs
    - FADH₂ produced (enters respiratory chain as e- donor)
    - 3 forms of mitochondrial Acyl-CoA dehydrogenase (short C4-8, medium C8-14 and long C12-18 chain FAs)
    - associated w/ inner membrane of mitochondria – feeds electrons into Complex II
  2. hydration of trans C=C (introduced in 1st reaction) to introduce C=O group on beta carbon atom
  3. another oxidation – at beta C to produce ketone (O=C-C-C=O) group instead of OH
    - formation of NADH
    - involves the enzyme 3-Hydroxyacyl-CoA dehydrogenase
  4. thioloysis
    - lysis of α-β C-C bond
    - addition of a coenzyme A moiety (group) to β carbon
    - production of acetyl-CoA
    - acyl-CoA produced can re-enter oxidation cycle
31
Q

What are the equations for the 4 stages of β-oxidation?

Hint - FeaTuring 3 different βAs

A
  1. fatty acyl CoA → trans-Δ₂-enoyl-CoA (acyl CoA dehydrogenase)
    - alongside: FAD → FADH₂
    - intro of a trans C=C bond betw/ α and β carbons
    - mitochondria have 3 versions of Acyl-CoA dehydrogenase (short, medium and long chain fatty acids)
  2. trans-Δ₂-enoyl-CoA → 3-L-Hydroxyacyl-CoA (enoyl-CoA hydratase)
    - alongside: hydration (+H₂O) of trans C=C → C=O
  3. 3-L-Hydroxyacyl-CoA → β-ketoacyl-CoA (3-hydroxyacyl-CoA dehydrogenase )
    - alongside: NAD⁺ + H⁺ → NAD⁺
    - oxidation to produce ketone (O=C-C-C=O) from C=O
  4. β-ketoacyl-CoA + CoA (moiety) → acyl-CoA + acetyl-CoA ( β-ketoacyl-CoA thiolase)
    - lysis of α-β C-C bond
    - produced Acyl-CoA which can re-enter oxidation cycle
  • then move into Complex III
32
Q

Give a summary of numbers of net products for the oxidation of long-chain, even-numbered, saturated fatty acids (e.g. palmitate).

A 
• beta oxidation:
- 7x NADH → 17.5x ATP
- 7x FADH₂ → 10.5x ATP
- 8x acetyl CoA 
↓
• citric acid cycle:
- 24xNADH → 60x ATP
- 8x FADH₂ → 12x ATP
- 8x GTP → 8x ATP
•  Total = 108x ATP per palmitoyl CoA
(see notes for diagram)
33
Q

What is ketogenesis?

Hint - ABAK

A
  • conversion: acetoacetate + β-hydroxybutyrate → acetyl-CoA → ketone bodies
  • cannot feed into citric acid cycle + drive ATP production
34
Q

Where is ketogenesis usually seen?

Hint - when there is some sort of problem

A
  • disease states of defective glucose metabolism/starvation (liver cells)
  • → lack of glucose metabolism
  • → oxaloacetate pyruvate (gluconeogenesis)
  • → reduced flux of CAC + acetyl-CoA accumulation
  • → excess acetyl-CoA provides energy in peripheral tissues (skeletal and cardiac muscle)
35
Q

What normally occurs with β-hydroxybutyrate in the body?

Hint - 2 conversions and then cut into CoAs and used for CACs

A
  • → (oxidised) to acetoacetate + succinyl-coA → acetoacetyl-CoA
  • next step cannot occur in liver cells (lack enzyme)
  • → (cleavage) acetoacetyl-CoA → 2x acetyl-coA → entry to citric acid cycle (mitochondria)
36
Q

How is ketogenesis caused and what are its symptoms and implications?

(Hint - high levels of 2 certain ketones, what this leads to; symptoms - Mikky Ekko song, getting crazy, GI pain)

A
  • too high levels of beta-hydroxybutyrate + acetoacetate in the blood can cause a drop in blood pH
  • occurs when more is produced than can be used by peripheral tissues
  • symptoms; nausea, vomiting, stomach pains, high acetone levels (fruity breath odour), delirium, comatose

(there are cases where diabetics with ketoacidosis have died)

37
Q

There are a range of different enzymes which work on overlapping chain lengths of fatty acyl-CoA. What is MCADD and its symptoms and treatment?

A
  • medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
  • inability to break down fat as an energy source
  • severity of enzyme deficiency is variable
  • symptoms: hypoglycaemia, build-up of medium length fatty acids, fatigue, seizures
  • treatment: feeding glucose regularly, enzyme replacement therapy

N&E (6 decks)

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