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Biochem BLOCK 2 > Pentose Phosphate pathway and NADPH > Flashcards

Pentose Phosphate pathway and NADPH Flashcards

1
Q

What’s another name for the pentose phosphate pathway?

A

Hexose MonoPhosphate Shunt

HMP shunt

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2
Q

What is the HMP shunt?

A

a branch off from the glycolytic pathway

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3
Q

what purposes does HMP shunt serve?

A
  • generation of NADPH

- generation of the 5-carbon sugar ribose, to be used in the synthesis of nucleotides

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4
Q

Does HMP shunt produce NADPH and ribose or one or the other?

A

can produce both or one or the other depending on the need of the cell

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5
Q

HMP shunt and ATP

A

NO ATP used or produced during this process

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6
Q

Step 1 of HMP shunt

A
  • dehydrogenation of glucose 6-P
  • enzyme Glucose 6-phosphate dehydrogenase (G6PD)
  • oxidative irreversible reaction
  • RATE LIMITING STEP
  • major point of regulation
  • the flux through the pathway increases in an absorptive state
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7
Q

glucose 6-phosphate dehydrogenase

A
  • enzyme for the dehydrogenation of glucose 6-P

- NADP+ is required enzyme

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8
Q

glucose 6-phosphate dehydrogenase inhibitor

A

NADPH is potent competitive inhibitor

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9
Q

expression of glucose 6-phosphate dehydrogenase

A

up-regulated by insulin

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10
Q

Step 2 of HMP shunt

A
  • hydrolysis to 6-phosphogluconate
  • enzyme-6-phosphogluconolactone hydrolase
  • IRREVERSIBLE
  • not rate limiting
  • produces 1 NADPH
  • oxidative
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11
Q

step 3 of HMP shunt

A

oxidative decarboxylation of 6-phosphogluconate

  • enzyme-6-phosphogluconate heydrogenase
  • IRREVERSIBLE
  • produces 1 NADPH
  • oxidative
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12
Q

steps 4-8 of HMP shunt

A
  • nonoxidative reversible reactions
  • interconversions of sugar molecules
  • interconvert sugars with 3-7C-atoms
  • permit synthesis of ribose 5-P used for nucleotide production
  • enzyme-transketolase
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13
Q

transketolase

A
  • requires TPP (from thiamine)
  • important in diagnosing thiamine deficiency
  • done by measurment of its activity in RBCs
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14
Q

structures of NADH and NADPH

A

very similar, just a small difference

-both e carriers, although not interchangeable

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15
Q

NADPH functions

A
  1. electron donor for the “reductive” biosynthesis of FA, cholesterol, and steroids
  2. E donor for the neutralization of reactive oxygen species
  3. provides reducing equivalents for cytochrome P450 monooxygenase system (for a biosynthesis of steroids and detox of xenobiotics)
  4. Play role in phagocytosis
  5. substrate for the synthesis of NO
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16
Q

NADPH role in neutralization of ROS

A
  • tripeptide: gamma-glutamylcysteinglycine (G-SH)

- Glutathion (GSH/GSSG) is the major antioxidant system

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17
Q

ROS produced

A
  • during aerobic metabolism
  • through reactions with drugs and toxins
  • when levels of antioxidants are diminished
18
Q

Monooxygenase

A

enzyme that will incorporate 1 O-atom from molecular oxygen (creating OH group) with the other being reduced to H2O

19
Q

Mitochondrial Ct P450

A
  • synthesis of steroids
  • inner mitochondrial membrane
  • steroidogenic tissue (placenta, ovaries, testes, adrenal cortex) uses NADPH for synthesis of steroid hormones
  • liver uses the same system to synthesize bile acids and vit D3
  • in kidney converts vit D3 to its active form
20
Q

Microsomal systme Cyt P450

A
  • membranes of smooth ER in liver cells
  • detox of drugs, toxins, chemicals
  • by adding O, the compound may be inactivated, made more soluble, or provide a reactive group (hydroxyl) for attachment of other compounds
21
Q

phagocytosis in WBC

A

neutrophils and mactophages (monocytes)

-generation of O free radicals aid in killing the microorganisms that the have engulfed

22
Q

The MPO system

A

combo of NADPH oxidase and myeloperoxidase are used to generate the O free radicals to aid in the destruction of microorganisms

23
Q

Chronic Granulomatous disease (CGS) caused by what?

A

rare genetic NADPH oxidase deficiency

24
Q

Chronic Granulomatous disease (CGS)

A
  • persistent serve infections due to the inability to kill bacteria forming granulomas
  • the granuloma is formed as a defense where the body attempts to “wall off” the collection of cells from the rest of the body
25
Q

Nitric oxide

A
  • NO
  • synthesized from argenine, oxygen, and NADPH
  • very short half-life
  • very reactive
  • diffuses into cells easily since it is a gas
26
Q

NO-synthase (NOS)

A

3 enzymes product of different genes

  • nNOS (neural tissues)
  • eNOS (endothelial cells)
  • iNOS (inducible)
27
Q

What NOS is constitutively expressed at constant levels?

A

nNOS

eNOS

28
Q

biological activity of NO

A
  • smooth muscle relaxant
  • used by macrophages to generate free radicals to kill microorganisms
  • inhibits platelet aggregation
  • functions as a neurotransmitter in brain
29
Q

nitroglycerin action

A

converted into NO to relax vascular smooth muscles

30
Q

Glucose 6-Phosphate dehydrogenase (G6PD) deficiency

A
  • inability to detoxify oxidizing agents

- some protection against malaria

31
Q

Where is the gene for G6PD?

A

on X chromosome (defects seen mostly in males)

-in some areas 25% of males are affected

32
Q

what populations have the highest incidence of G6PD deficiency?

A

african, mediterranean, asian

33
Q

What is the incidence of G6PD among american blacks?

A

11%

34
Q

G6PD deficiency precipitating factors

A

usually only symptomatic when experiencing an oxidative stress

  • infection (O radicals generated by macrophages)
  • drugs that produce an oxidative stress
  • fava beans (only some deficiencies) also called favism
35
Q

clinical manifestations of G6PD deficiency

A
  • almost exclusively in RBCs as an episodic hemolytic anemia in adults
  • neonatoal jaundice in newborns
  • effects on other organs/tissues are due to hemolytic anemia
  • shortened life span in individuals with the severe form
36
Q

Why G6PD deficiency in RBCs?

A
  • BC in RBCs, the only pathway to make NADPH is via the HMP pathway
  • in other cell types, other pathways contribute to NADPH formation
  • RBCs cannot synthesize more G6PD because they have no nucleus.
37
Q

Most of the mutations that result in G6PD deficiency …

A

affect the stability of the enzyme, which means over the life cycle of a RBC the enzyme is lost and not replaced

38
Q

characteristic of G6PD deficiency in RBCs

A

presence of Heinz bodies in RBCs

39
Q

Heinz bodies

A

precipitates of oxidized hemoglobin in RBCs

40
Q

recovery from G6PD deficiency

A

if oxidative stress is removed, usually the patient will recover as new RBCs are made

Biochem BLOCK 2 (14 decks)

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