- Oxidises glucose (6C) to produce 2NADH, 2ATP and 2 pyruvate (2 x 3C)

L7- Glycolysis Flashcards by Saskia Chapman

glycolysis simple

Oxidises glucose (6C) to produce 2NADH, 2ATP and 2 pyruvate (2 x 3C)

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what type of pathway is glycolysis

irreversible

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glycolysis is not isolated and has important intermediates that get fed into other pathways e.g.

Dihydroxyacetone- P

2,3- Bis phosphoglycerate

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Dihydroxyacetone- P comes from

comes from the 5th enzyme of glycolysis (glyceraldehyde-3-P)

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Dihydroxyacetone- P is converted into ………. by …….

glycerol phosphate by glycerol-3-phosphate dehydrogenase via oxidation of NADH ==> NADH+

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glycerol phosphate important

in triglyceride and phospholipid biosynthesis

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where is GP produced

adipose and liver

lipid synthesis in adipose requires glycolysis

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2,3-bisphosphate (2,3 BP)comes from …….. by ……

1,3- bisphosphoglycerate by 2,3-bisphosphoglycerate mutase

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where is 2,3-bisphosphate (2,3 BP)produced

RBC

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what is 2,3-bisphosphate (2,3 BP) a regulator of

haemoglobin O2 affinity

promotes release of O2 to tissue
present in RBC at same molar conc as Hb (5mM)

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what is GP produced from

DHAP found in adipose and liver

liver can phosphorylate glycerol directly

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glycolysis requires

NAD+ to produce pyruvate

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total [NAD+ and NADH] is

constant in the cell

o Glycolysis would stop when all NAD+ is converted to NADH
o Normally, NAD+ is regenerated from NADH in stage 4 of metabolism

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glycolysis in RBC

have now stage 3 or 4 of metabolism (no mitochondria)

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stage 4 (ETC) needs

oxygen

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supply of O2 to muscles and gut is often

reudced

- therefore need way of regretted NADh by some other route

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RBC, muscles and gut need way of

regenerating NAD+

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what alternative pathway can use to to regenerate NAD+ int issue which lack oxygen/ cells which have no ETC

Lactate dehydrogenase (LDH)

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lactate dehydrogenase

converts NADH + H + pyruvate –> NAD+ and lactae

regenerating NAD+ source to be used in glycolysis

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lactate is produced from

glucose and alanine via pyruvate

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without major exercise (lactate production)

o 40-50g/24 hours

 RBC, skin, brain, skeletal muscle, GI tract

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strenuous exercise (lactate production)

o 30g/5 mins
 Plasma levels x 10 in 2-5 min
 Back to normal by 90 mins

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pathological situations v

o High
 Shock
 Congestive heart disease

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LDH is produced by

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RBC and skeletal muscle, skin, brain, GI (need lots of oxygenp- storage of NAD+)

LDH is released into blood and metabolised by

liver nad heart

liver and heard need NAD+ to be

regenerated efficiently- well supplied with oxygen

in low o2 conditions pyruvate con Crete duo

lactate instead of stage 4 of metabolism (which enquires oxygen) by lactate dehydrogenase

in the liver and kidney LDH converts lactate to

pyruvate

plasma conc of lactate determined by

1. rate of production 2. rate of utilisation (liver, RBC, heart, muscle) 3. rate of disposal (kidney)

hyperlactaemia

- 2-5 mM - below renal threshold - no change in blood pH (buffering capacity)

lactic acidosis

above 5mM - above renal threshold - blood pH lowered

normal conc of lactate

,1mM

lactose acidosis is a critical markers of

acutely unwell patient

metabolism of other sugars e.g.

fructose and galactose

fructose

Found in fruit (monosaccharide)- forms sucrose disaccharide with glucose (2xC3) - Metabolised in liver in human

fructose enters glycolysis as

G-3-P | as opposed to glucose which enters as G-6-P

clinical important of fructose metabolism

1. essential fructosuria | 2. fructose intolerance

essential fructosuria

o Fructose kinase missing | o Fructose found in urine no clinical signs

fructose intolerance

o Aldolase missing o Fructose-1-P accumulates in liver - Leading to liver damage

treatment of fructose intolerance

Treatment- remove fructose from diet

galactose

monosaccharide that can form a disaccharide with glucose to form lactose

lactose is a

disaccharide found in milke

deficiency in which three main enzymes (only one needs to be deficient) causes galactosaemia

- galactokinase - UDP- galactose epimerase - Uridyl transferase

galactosaemia causes how many deaths

1 in 30,000

galactokinase deficiency is

rare

what does galactokinase deficiency cause

galactose accumulates

transferase deficiency is

common

what does transferase deficiency cause

galactose 1-p accumulate

problem with galactose accumulation

depletes NADPH levels

lens related problem with depletion of NADPH

o Prevents maintenance of free sulfhydryl groups on proteins o Inappropriate disulphide bond formation o Loss of structural and functional integrity of some proteins that depend on free -SH groups  Cataracts

accumulation of galactose 1-p affects

liver, kdineha nd rbain

treatment of galactosaemia

no lactose in diet

the pentose pathway role

providing NADPH to maintain SH groups of proteins in a reduced state - Structural integrity and functional activity of some proteins depends on free-SH groups

pentose phosphate pathway starts from

glucose-6- phosphate

lentos phosphate pathway important

- Important source of NADPH required for o Reducing power for biosynthesis (NADPH) o Maintenance of GSH levels o Detoxification reactions - Produces C5-sugar ribose required for synthesis of: o Nucleotides o DNA and RNA

glucose- 6- phosphate dehydrogenase deficiency (G6PDH)

is v common inherited defect o E.g. in RBC, reduced NADPH  inappropriate disulphide bonds formed  aggregated proteins (Heinz bodies)  haemolysis e.g. lens of eye

glucose- 6- phosphate dehydrogenase is a .... enzyme

rate limiting

product to pentose phosphate pathway

5C sugar ribose, NADPH, CO2

is ATP produced in PPP

L7- Glycolysis Flashcards

(59 cards)