Amino Acid Synthesis Flashcards

1
Q

What kind of aa’s are essential?

A

Ones that we cannot synthesize ourselves

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2
Q

What are the two pseudo-essential aa’s?

A

Arg - insufficient in infants

Met - can be recycled

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3
Q

What two things do most Non-essential amino acids need?

A

NADPH and ATP

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4
Q

What is considered a risk factor for CVD?

A

Elevated serum homocysteine levels

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5
Q

What may result in elevated serum homocysteine levels?

A

Deficiencies in THF, B12 or B6

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6
Q

What amino acids are synthesized by direct transaminations?

A

Ala from Pyr
Asp from OAA
Glu from alpha-KG

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7
Q

How is proline synthesized?

A

By the reversal of Proline catabolization to Glu

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8
Q

How is Tyrosine made?

A

By hydroxylation of phenylalanine catalyzed by phenylalanine hydroxylase

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9
Q

What is Phenylalanine hydroxylase?

A

A mixed function oxidase

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10
Q

Are neurotransmitters transient?

A

Yes

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11
Q

Which NT’s are rapidly degraded or altered in the synaptic cleft?

A

ACh via Acetylcholinesterase
Norepinephrine via monoamine oxidase
Dopamine via monoamine oxidase

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12
Q

What neurotransmitter get’s endocytosed?

A

Serotonin

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13
Q

What is ACh derived from??

A

Serine

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14
Q

What does botox do to ACh?

A

Blocks ACh secretion

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15
Q

What does Cognex do to ACh?

A

Slows acetylcholinesterase

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16
Q

What does Sarin do to ACh?

A

Blocks acetylcholinesterase

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17
Q

What does Atropine do to ACh?

A

Blocks acetylcholine receptor

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18
Q

What is GABA derived from?

A

Glutamate which is decarboxylated

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19
Q

What type of NT is GABA and how does it act?

A

It is an inhibitory NT that acts by increasing K+ permeability of post-synaptic neuron

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20
Q

In what cases is GABA decreased?

A

Huntington’s chorea

Epilepsy

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21
Q

What increases GABA?

A

Valium
Librium
Alcohol

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22
Q

What thyroid hormones come from Tyrosine?

A

T3

T4

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23
Q

What NT’s/Hormones come from Tyrosine?

A

DOPA
Dopamin
Norepinephrine
Epinephrine

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24
Q

What pigment compounds come from Tyrosine?

A

Melanin

25
Q

What is Serotonin derived from?

A

Tryptophan which is hydroxylated then decarboxylated

26
Q

How does Serotonin affect the body?

A

A potent vasoconstrictor in brain, platelets and mast cells

A major regulator of mood in the CNS

27
Q

What can Serotonin be converted into?

A

Melatonin in the pineal gland (Makes you sleepy)

28
Q

What increases serotonin levels?

A

SSRIs like Prozac and Zoloft

29
Q

What is tryptophan a precursor for?

A

Nicotinate (niacin), the ring portion of NAD and NADP

30
Q

What is Histamine derived from?

A

Histidine which is decarboxylated

31
Q

What is histamine secreted by?

A

Mast cells
Lung
Gastric Mucosa

32
Q

What’s the function of histamine?

A

It’s a potent vasodilator

33
Q

What is Tagamet?

A

An H2 receptor agonist with similar structure to histamine

34
Q

NO derived from what aa?

A

Arginine via the enzyme nitric oxide synthase

35
Q

What is the function of NO?

A

It’s a potent vasodilator

36
Q

What 3 aa’s make Glutathione(GSH)?

A

Glu
Cys
Gly

37
Q

What kind of reducing agent is GSH?

A

A strong one

38
Q

Is there a gene or mRNA for GSH?

A

Nope

39
Q

What 3 aa’s make Creatine Phosphate?

A

Arg
Gly
Met

40
Q

What does Creatine Phosphate phosphorylate?

A

ADP > ATP

41
Q

What can store phosphate with increasing ATP levels as a result of Creatine Phosphate?

A

Muscle and Cardiac

42
Q

What can creatine phosphate be metabolized into?

A

Creatinine

43
Q

What does increased excretion of creatinine indicative of?

A

Kidney Damage

44
Q

What are polyamides made from?

A

Ornithine

45
Q

When do polyamines with DNA ?

A

During compaction

46
Q

What is carnitine made from?

A

Trimethyllysine

47
Q

How does carnitine act as an acyl group carrier?

A

Picks up acyl in cytoplasm, transfers to CoA in mitochondria then free carnitine returns to cytoplasm

48
Q

Where is heme primarily synthesized?

A

Primarily in liver and bone

49
Q

What are porphyrias?

A

Diseases of heme synthesis

50
Q

What is congenital erythropoietic porphyria?

A

A defect in the enzyme cosynthase which results in large amounts of uroporphyrinogen I.

51
Q

What are the symptoms of congenital erythropoietic porphyria?

A

Premature destruction of RBC’s
Red Urine
Teeth have strong red fluorescence
Skin Sensitive to Light

What are you a Vampire?

52
Q

What is acute intermittent porphyria?

A

A defect in the enzyme uroporphyrinogen I synthase.

53
Q

What are the symptoms of acute intermittent porphyria?

A

Dark urine (primarily liver defect)
Episodic bouts of irrational behavior
Paralysis or severe pain
Hypertension

54
Q

What is toxic porphyria?

A

Chemical induced by drugs like Phenobarbital

55
Q

Where do RBC’s break down?

A

In the spleen where they release heme

56
Q

What does heme degrade into?

A

Biliverdin, CO and free FE2+

57
Q

What does Biliverdin get converted into?

A

Bilirubin which is carried by albumin through the bloodstream to the liver

58
Q

What is bilirubin converted into and where is it excreted?

A

It is converted into bilirubin diglucuronide for excretion into the small intestine with bile.

59
Q

What does Liver damage or blocked bile ducts result in?

A

Jaundice