1
Q

what is aerobic respiration and where does it take place?

A

→Aerobic respiration is the process of producing cellular energy involving oxygen.
→ it occurs ONLY in the presence of oxygen
→ 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

what are the steps in the citric acid cycle?

A

→Pyruvate (3C) is converted to Acetyl CoA (2C), releasing a CO2 molecule and an NADH molecule.

→This is done by the enzyme Pyruvate Dehydrogenase.

→ Acetyl CoA (2C) is then joined with Oxaloacetate (4C) to make citric acid (6C).

→This is done by the enzyme Citrate Synthase.

→ Citric Acid (6C) is then converted to Isocitrate (6C).

→Isocitrate (6C) is then converted to α-ketoglutarate (5C) by Isocitrate Dehydrogenase. This releases a molecule of CO2 and NADH.

→ α-ketoglutarate (5C) is converted to Succinyl CoA (5C) by α-ketoglutarate dehydrogenase. This, again, releases a molecule of CO2 and NADH.

→Succinyl CoA (5C) is converted to Succinate (4C), releasing GTP.

→ Succinate (4C) is then converted to Fumarate (4C), releasing FADH2.

→Fumerate (4C) is converted to Malate (4C).

→ Malate (4C) is finally converted to Oxaloacetate (4C), releasing NADH.

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3
Q

what does pyruvate dehydrogenase do and what is it inhibited and stimulated by?

A

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

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4
Q

what does citrate synthase do and what is it inhibited by?

A

→joins Oxaloacetate and Acetyl CoA to make Citrate

→ inhibited by citrate

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5
Q

what does isocitrate dehydrogenase do and what is it inihbited and stimulated by

A

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

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6
Q

what does α ketoglutarate dehydrogenase do and what is it inhibited by?

A

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

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7
Q

how many molecules of FADH and NADH and GTP are made in every citric acid cycle?

A
→FADH2 = 1
→NADH = 3
→GTP  = 1
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8
Q

what regulates entry into the citric acid cycle?

A

→ 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.

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9
Q

how is pyruvate dehydrogenase activated in muscles?

A

→In muscles, Pyruvate Dehydrogenase is activated again via the action of a phosphatase; this enzyme is stimulated by Ca2+ (this increases CoA production)

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10
Q

how do calcium levels increase in the liver?

A

→In the liver, adrenalin increases calcium through the activation of α-adrenergic receptors and IP3

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11
Q

how is phosphatase stimulated in the liver?

A

→ In the liver and adipose tissue, insulin (which signifies the fed state) stimulates the phosphatase, which funnels glucose to Fatty Acid synthesis

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12
Q

what is beri beri?

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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13
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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14
Q

how does ATP Synthase generate ATP?

A

→due to the H+ gradient created, the ions now move back down into the matrix of the mitochondria through ATP Synthase down their electrochemical gradient

→This movement generates enough energy for it to combine ADP and phosphate into ATP.

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15
Q

why do newborn babies need brown fat and where is this distributed?

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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16
Q

what are OXPHOS Diseases and what are the symptoms?

A

→Common degenerative diseases

→Caused by mutations in genes encoding proteins of ETC

→Lead to a number of symptoms, including fatigue, epilepsy, dementia

→dependent on the mutation, symptoms may be evident near birth to early adulthood

→Metabolic consequence can be congenital lactic acidosis