Energy II Flashcards

1
Q

Describe aerobic respiration.

A

Aerobic respiration is the process of producing cellular energy involving oxygen.

  • it occurs ONLY in the presence of oxygen (obviously)
  • it yields more energy than anaerobic respiration in the form of ATP (around 38)
  • it takes place in the mitochondria
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2
Q

Describe the entire citric acid cycle.

A

1) Pyruvate (3C) is converted to Acetyl CoA (2C), releasing a CO2 molecule and an NADH molecule. This is done by the enzyme Pyruvate Dehydrogenase.
2) Acetyl CoA (2C) is then joined with Oxaloacetate (4C) to make citric acid (6C). This is done by the enzyme Citrate Synthase.
3) Citric Acid (6C) is then converted to Isocitrate (6C).
4) Isocitrate (6C) is then converted to α-ketoglutarate (5C) by Isocitrate Dehydrogenase. This releases a molecule of CO2 and NADH.
5) α-ketoglutarate (5C) is converted to Succinyl CoA (5C) by α-ketoglutarate dehydrogenase. This, again, releases a molecule of CO2 and NADH.
6) Succinyl CoA (5C) is converted to Succinate (4C), releasing GTP.
7) Succinate (4C) is then converted to Fumerate (4C), releasing FADH2.
8) Fumerate (4C) is converted to Malate (4C).
9) Malate (4C) is finally converted to Oxaloacetate (4C), releasing NADH.

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3
Q

List the 4 enzymes we need to know that are involved in the citric acid cycle, and list what inhibits them.

A

PYRUVATE DEHYDROGENASE:

  • converts Pyruvate to Acetyl CoA
  • inhibited by NADH, ATP, Acetyl CoA
  • stimulated by ADP and Pyruvate

CITRATE SYNTHASE:

  • joins Oxaloacetate and Acetyl CoA to make Citrate
  • inhibited by Citrate

ISOCITRATE DEHYDROGENASE:

  • converts Isocitrate to α-ketoglutarate
  • inhibited by NADH and ATP
  • stimulated by ADP

α-KETOGLUTARATE DEHYDROGENASE:

  • catalyses the conversion of α-ketoglutarate to succinyl-CoA
  • inhibited by NADH, ATP and Succinyl CoA
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4
Q

How many ‘energy molecules’ are made in every citric acid cycle?

A

NADH: 3
FADH2: 1
GTP: 1

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5
Q

What regulates entry into the citric acid cycle?

A

The formation of Acetyl CoA from Pyruvate (by Pyruvate Dehydrogenase) is irreversible. This commits the glucose carbon skeleton to either oxidation to CO2 and energy production or fatty acid synthesis.

  • In muscles, Pyruvate Dehydrogenase is activated again via the action of a phosphatase; this enzyme is stimulated by Ca2+ (this increases CoA production)
  • In the liver, adrenalin increases calcium through the activation of α-adrenergic receptors and IP3
  • In the liver and adipose tissue, insulin (which signifies the feed state) stimulates the phosphatase, which funnels glucose to Fatty Acid synthesis
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6
Q

Describe Beriberi.

A

It’s a disease in which the body has a deficiency in thiamine (Vit B1). Thiamine is a prosthetic group for pyruvate and α-ketoglutarate dehydrogenase.
It’s characterised by cardiac and neurological symptoms (impairment of nerves and heart).
It’s common where rice is a staple. Neurological disorders are common as glucose is a primary source of energy.

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7
Q

What happens to the NADH and FADH2 produced?

A
  1. Oxidative Phosphorylation starts with 3 NADH and 1 FADH2 being added. NADH transfers its high energy molecules to Protein Complex 1 (NADH Dehydrogenase), while FADH2 transfers its high energy molecules to Protein Complex 2 (Succinate Dehydrogenase). This causes a loss of electrons (oxidation). This also converts them to their oxidated forms, NAD+ and FAD+.
  2. The process of NADH oxidation leads to the pumping of protons through Protein Complex 1 from the matrix to the inner membrane space. These electrons are then transferred to another membrane-bound electron carrier called Ubiquinone (Q/ Coenzyme Q). FADH2 simply transfers its electrons to Q; no hydrogen pumping occurs.
  3. Inside the nonpolar region of the phospholipid bilayer, UQH2 (which is also a nonpolar compound) transports the electrons to Protein Complex 3 (Cytochrome b-c1). UQH2 also carries protons. When UQH2 delivers electrons to Protein Complex 3, it also donates its protons to be pumped.
  4. The electrons that arrived at Protein Complex 3 are picked up by Cytochrome C (or “cyt C”), the last electron carrier. This action also causes protons to be pumped into the inner membrane space.
  5. Cytochrome C carries the electrons to the final protein complex, Protein Complex 4 (Cytochrome Oxidase). Once again, energy released via electron shuttling allows for another proton to be pumped into the inner membrane space. The electrons are then drawn to oxygen, which is the final electron acceptor. Its important to note that oxygen must be present for oxidative phosphorylation to occur. Water is formed as oxygen receives the electrons from Protein Complex 4, and combines with protons on the inside of the cell.
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8
Q

How many ATP molecules are produced each from NADH and FADH2?

A

For every NADH molecule, 3 ATP molecules are formed.

For every FADH2 molecule, 2 ATP molecules are formed.

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9
Q

How does ATP Synthase generate ATP?

A

Due to the H+ gradient created, they now move back down into the matrix of the mitochondria through ATP Synthase. This movement generates enough energy for it to combine ADP and phosphate into ATP.

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10
Q

Why do newborn babies need brown fat?

A

Newborn babies can’t shiver, so they have brown fat (brown due to the high levels of mitochondria). High levels of brown fat in newborns provides an alternative way of regulating heat, to protect them from hypothermia. The brown fat is distributed around the shoulders and down the back. As they grow, the amount of brown fat they have decreases.

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11
Q

What are Oxphos Diseases?

A

They are common degenerative diseases. They’re caused by mutations in genes encoding proteins of the ETC. They lead to a number of symptoms, such as fatigue, epilepsy, dementia, etc. It’s dependant on the mutation, and symptoms may be evident near birth to early adulthood. One metabolic consequence can be Congenital Lactic Acidosis (CLA, a rare disease that affects the cells ability to use energy and causes a build up of lactic acid).

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