Pentose phosphate pathway

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The pentose phosphate pathway

The pentose phosphate pathway (also called the phosphogluconate pathway and the hexose monophosphate shunt and the HMP Shunt) is a

nucleotides.[2] While the pentose phosphate pathway does involve oxidation of glucose, its primary role is anabolic rather than catabolic. The pathway is especially important in red blood cells (erythrocytes). The reactions of the pathway were elucidated in the early 1950s by Bernard Horecker and co-workers.[3][4]

There are two distinct phases in the pathway. The first is the

oxidative phase, in which NADPH is generated, and the second is the non-oxidative synthesis of 5-carbon sugars. For most organisms, the pentose phosphate pathway takes place in the cytosol; in plants, most steps take place in plastids.[5]

Like

metal ions, particularly ferrous ions (Fe(II)).[6]
This suggests that the origins of the pathway could date back to the prebiotic world.

Outcome

The primary results of the pathway are:

Aromatic amino acids, in turn, are precursors for many biosynthetic pathways, including the lignin in wood.[citation needed]

Dietary pentose sugars derived from the digestion of nucleic acids may be metabolized through the pentose phosphate pathway, and the carbon skeletons of dietary carbohydrates may be converted into glycolytic/gluconeogenic intermediates.

In mammals, the PPP occurs exclusively in the cytoplasm. In humans, it is found to be most active in the liver, mammary glands, and adrenal cortex.[

reducing power, accounting for approximately 60% of NADPH production in humans.[citation needed
]

One of the uses of NADPH in the cell is to prevent oxidative stress. It reduces glutathione via glutathione reductase, which converts reactive H2O2 into H2O by glutathione peroxidase. If absent, the H2O2 would be converted to hydroxyl free radicals by Fenton chemistry, which can attack the cell. Erythrocytes, for example, generate a large amount of NADPH through the pentose phosphate pathway to use in the reduction of glutathione.

phagocytes in a process often referred to as a respiratory burst.[7]

Phases

Oxidative phase

In this phase, two molecules of

glucose-6-phosphate into ribulose 5-phosphate
.

Oxidative phase of pentose phosphate pathway.
Glucose-6-phosphate (1), 6-phosphoglucono-δ-lactone (2), 6-phosphogluconate (3), ribulose 5-phosphate (4)

The entire set of reactions can be summarized as follows:

Reactants Products Enzyme Description
Glucose 6-phosphate + NADP+ →
6-phosphoglucono-δ-lactone
+ NADPH
glucose 6-phosphate dehydrogenase
NADPH
is generated.
6-phosphoglucono-δ-lactone
+ H2O		 →
6-phosphogluconate
+ H+		 6-phosphogluconolactonase Hydrolysis
6-phosphogluconate
+ NADP+		 → ribulose 5-phosphate + NADPH + CO2
6-phosphogluconate dehydrogenase
 Oxidative
NADPH, a CO2, and ribulose 5-phosphate
.

The overall reaction for this process is:

Glucose 6-phosphate + 2 NADP+ + H2O → ribulose 5-phosphate + 2 NADPH + 2 H+ + CO2

Non-oxidative phase

The pentose phosphate pathway's nonoxidative phase
Reactants Products Enzymes
ribulose 5-phosphate → ribose 5-phosphate ribose-5-phosphate isomerase
ribulose 5-phosphate → xylulose 5-phosphate ribulose 5-phosphate 3-epimerase
xylulose 5-phosphate + ribose 5-phosphate → glyceraldehyde 3-phosphate + sedoheptulose 7-phosphate transketolase
sedoheptulose 7-phosphate + glyceraldehyde 3-phosphate → erythrose 4-phosphate + fructose 6-phosphate transaldolase
xylulose 5-phosphate + erythrose 4-phosphate → glyceraldehyde 3-phosphate + fructose 6-phosphate transketolase

Net reaction: 3 ribulose-5-phosphate → 1 ribose-5-phosphate + 2 xylulose-5-phosphate → 2 fructose-6-phosphate + glyceraldehyde-3-phosphate

Regulation

acetyl CoA.[citation needed
]

oxidative damage or support de novo lipogenesis.[9][10]

Erythrocytes

Several deficiencies in the level of activity (not function) of glucose-6-phosphate dehydrogenase have been observed to be associated with resistance to the malarial parasite Plasmodium falciparum among individuals of Mediterranean and African descent. The basis for this resistance may be a weakening of the red cell membrane (the erythrocyte is the host cell for the parasite) such that it cannot sustain the parasitic life cycle long enough for productive growth.[11]

See also

References

  1. PMID 32664469
    .
  2. PMID 32664469
    .
  3. PMID 14907726
    .
  4. PMID 12403765
    .
  5. PMID 12753973
    .
  6. PMID 24771084
    .
  7. ^ Immunology at MCG 1/cytotox
  8. ISBN 978-0-470-57095-1
    .
  9. PMID 24769394
    .
  10. PMID 27586085
    .
  11. PMID 9746794
    .

External links
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