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Metabolism > Pentose phosphate pathway > Flashcards

Pentose phosphate pathway Flashcards

1
Q

what is the pentose phosphate pathway

A
  • completely different pathway of glucose oxidation
  • aka the hexose monophosephate shunt
  • oxidation WITHOUT ATP production
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2
Q

purpose of the pentose phosphate pathway

A
  • supplies ribose-5-phosphate for nucelotide and nuceil acid synthesis
  • supplies reducing power as NADH for synthesis of fat, cholesterol, steroids etc
  • provides route for excess pentose sugar inthe diet into mainstream metabolism
  • recycles sugars according to the needs of the cell
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3
Q

two phases of the PPP

A

oxidative and non-oxidative

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4
Q

why doesnt PPP produce ATP

A

because the NADPH doesn’t go to the mitochondria and ETC

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5
Q

where does PPP occur

A

mainly in the cytosol of cells, along with glycolysis

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6
Q

where are PPP enzymes most plentiful

A
  • in tissues with high demand for NADPH for synthesis
  • rapidly dividing cells which require ribose-5-phosphate for DNA synthesis
  • in the liver, because the main demand is for FA synthesis
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7
Q

quantitatively, what is the main demand of PPP

A

FA synthesis

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8
Q

PPP in skeletal muscle

A

very little activity

but because PPP produces ribose-5-phosphate, all tissues are likely to have some activity

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9
Q

why do mature erythrocytes need the PPP

A

they require NADH to maintain the cell membrane integrity

- maintains the reduced environment to stop bursting

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10
Q

which part of PPP is irreversible and produces ribose-5-phosphate and NADPH

A

oxidative

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11
Q

steps of the oxidative PPP

A
  • G6P converted to 6-phosphgluconate
  • NADP+ reduced to NAPDH
    enzyme: glucose-6-dehydrogenase
  • 6-phosphogluconate dehydrogenase reduces NADP+ and generates beta-keto-acid
  • beta-keto-acid decarboxylated to keto-pentose-ribulose-5-phosphate
  • isomerase converts keto-pentose-ribulose-5-phosphate into aldose isomer: riose-5-phosphate
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12
Q

what controls the oxidate part of PPP

A

rate limiting step: oxidation of G6P to 6-phosphogluconolactone, by enzyme glucose-6-dehydrogenase

rate of reaction is tightly coupled to [NAD+] which governs the allocation of G6P to PPP instead of glycolysis

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13
Q

non oxidative part of PPP

A
  • Interconverts sugars according to needs of cells

- involves transaldose and transketolases

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14
Q

what do transaldose and transketolase do in the non-oxidative part of PPP

A

detach C3 and C2 respectively from ketose sugar phosphate, and transfer them other aldose sugars

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15
Q

what is the thiamin (B1) pyrophosphate-dependent enzyme

A

transketolase (like in the link reaction)

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16
Q

when do tissues demand high NADPH

A

during fat synthesis

  • production of NADPH for fat synthesis also results in increased ribose-5-phosphate
  • there might be more R5P than cell needs for nucleotide synthesis
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17
Q

when do tissues demand high R5P

A

rapidly dividing cells that arent synthesizing fat, have high requirement for R5P but not NADPH

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18
Q

how do requirements for NADPH and R5P alter

A

vary with different tissue demands
the demand for R5P and NADPH can be equal, or weighted to one more than the other

production is controlled by the non-oxidatve part of the pathway

19
Q

what controls balance of NADPH and R5P production

A

non-oxidative part of PPP

20
Q

Oxidative balance equation

A

G6P + 2NADP+ + H2O –> R5P + 2NADPH + 2H+ + CO2

21
Q

when is the non-oxidative part of PPP not needed

A

when the oxidative part is balanced

22
Q

When does conversion of R5P to X5P occur

A

when the liver needs 2NADPH but does not need the R5P of the balance equation
- phosphophentose isomerase and epimerase

23
Q

X5P

A

xylulose 5 phosphate

24
Q

what else does R5P get converted to when in excess

A

R5P to glyceraldehyde3P and F6P

  • these can enter glycolysis or gluconeogenesis
  • F6P can also be converted to G6P and reenter PPP

occurs by 3 reactions using transketolase, transaldolase and transketolase again

25
Q

conversion of surplus R5P into G6P: when and how

A

if non dividing cell requires more NADPH than R5P

the non-oxidative part recycles excess into G6P
6 R5P -> 5 G6P + Pi

26
Q

conversion of R5P into glyceraldehyde-3-phosphate: why

A

G3P can then be converted to G6P by gluconeogenesis reactions

27
Q

6 C5 sugars are converted to

A

5 x G6P

(3 R5P and 3 XYP

28
Q

conversion of G6P into R5P without NADPH generation : summary

A

if a cell needs R5B for nuceotide synthesis but has little demand for NADPH:
G6P + ATP -> 6R5P + ADP + Pi

  • where R5P is required and NADH isnt
  • oxidative part of PPP doesn’t operate
  • glycolytic intermediates are converted to R5P by transketolase and transaldolase enzymes
29
Q

steps of conversion of G6P into R5P without NADPH generation

A
  • G6P is converted by glycolytic pathway partly in F6P an partly into glyceraldehyde3P
    = C3 and C6 products
  • reversal of the these steps produces X5P which is isomerised to R5P
30
Q

why is the PPP important for erythrocyte

A
  • mature erythrocytes do not divide
  • no need for R5P for nuclei synthesis or fat synthesis bc they derive energy from glycolysis
    BUT they need a supply of NADPH to protect cell membrane from oxidative damage
31
Q

Protective effect of NADPH on erythrocytes

A
  • RBC membrane is subject to attack by H2O2
  • H2O2 needs to be detoxified
  • 2 reduced GSH attack H2O2 to make water and the GSH become oxidised to GSSG
  • GSSG is useless so FAD re-reduces to farm GSH again
  • NADPH is needed to activate the GSSG to GSH
32
Q

Main function of glutathione

A

to maintain reducing environemnt in cells by virtue of its -SH group (thiol)
AHA GSH

33
Q

why are RBC susceptible to oxidative damage

A
  • high O2 content in cell gives rise to harmfel ree radicals or ROS
  • RBC depend on GSH for integrity
  • GSH reduces ferrihaemoglobin to ferrous form
  • GHS destroys H2O2
  • GSH regenerates reduction environemnt using NADPH
34
Q

why does RBC depend on GSH

A
  • GSH reduces ferrihaemoglobin to ferrous form
  • GHS destroys H2O2
  • GSH regenerates reduction environemnt using NADPH

therefore continuous supply of NADPH is also key

35
Q

GSH

A

glutathione

36
Q

what is the only way of generating NADPH and GSH inthe cell

A

PPP and hence vital for RBC

37
Q

G6P dehydrogenase deficiency

A

most common human enzyme disorder

  • X-linked hereditary disorder so most asymptopic
  • symptopic patients usally male
  • more than 400mil worldwide are G6PD deficient, mostly in Africa, middle East and south Asia
38
Q

what happens to people with G6PD

A

they can be completely OK until ertythrocyte is challenged with oxidation

= haemolytic anaemia

39
Q

triggers for haemolytics anaemia

A
  • favism
  • infection
  • oxidant drugs
40
Q

favism

A

ingestion of fava beans

  • some forms of G6PD, particulary mediterraneon varient, are particulary susceptible to favism
  • fava beans contain alkaloids such as vicine which are potent oxidants
41
Q

infection triggering haemolytic anaemia

A

inflammatory response to infection can lead to generationof oxidatns such as fre radicals, which enter E and cause haemolysis

42
Q

oxidant drugs triggering haemolytic anaemia

A

antimalaria drugs; chloroquine can be harmful
- indivuduals should be tested for G6PD before being prescribed these

  • sulphonamides, sulfa antiobiotics and analgesics should also be avoided
43
Q

sidelight of G6PD

A

selective advantage in areas where lethal type of malaria is endemic
possible reasons:
- parasite had requirement for products of PPP
- AND/OR extra stress by parasite causes the deficient RBC host to lyase before parasite completes development (doesnt live usual 120 days)

similar to sickcell - potentially lethal disease that provides survival advantage against an even more lethal disease

Metabolism (11 decks)

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