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18 Cards in this Set

  • Front
  • Back
Glucose 6-P Dehydrogenase Deficiency
-Arise upon administrating antimalarials or sulfa antibiotics
-Patients have hemolytic anemia
-Cells do not reduce enough NADP+ to maintain glutathione in its reduced state for their cell membrane.
Purpose of the PPP?
-NADPH Production (reducing power)
-Production of ribose-5-P to make DNA and RNA
PPP overall pathway
1-glucose-6-P + 2NADP + 2H2O ---> 2 NADPH (reduced) + Ribose 5-P + CO2
1. Glucose-6-P ---> 6-Phosphogluconolactone (6-PGL)
Glucose-6-P Dehydrogenase + NADPH
-First committed step
-Regulated by NADPH
2. 6-Phosphogluconolactone (6-PGL) --->6-phosphogluconate
-converts cyclic structure to linear structure
3. 6-Phosphogluconate ---> Ribulose-5-Phosphate
6-Phosphogluconate Dehydrogenase + NADPH + CO2
4. Ribulose-5-P ---> Ribose-5-P
Ribulose-5-P isomerase
If need to make NADPH + Ribose-5-P
-Do oxidative stage only
-Use ribose 5-P for DNA, RNA, NADPH
If need to make NADPH only
Use whole pathway (oxidative and nonoxidative stage)
-Swap Carbons using Transketolases and Transaldolases to get glyceraldehyde 3-P and 2 moles of Fructose 6-P
-Feed to the top to produce NADPH
NADPH + energy
Whole pathway + glycolysis
Ribose-5-P only
-Runs in reverse
-Take Glyceraldehyde-3-P and Fructose-6-P to produce Ribose-5-P using TA and TK
Transketolase (TK)
Take 2 carbons from Ketose to Aldose
-cofactor: Thiamine PP
Transaldolase (TA)
3 carbons from ketose to aldose
Glucose-6-P dehydrogenase deficiency
-Oxidative stress (antimalarial drugs, infection, flava beans), hemolytic anemia
-Need NADPH to give reduced glutothione which keeps Hb reduced and rbc membrane intact
Thiamine Deficiency (beri beri)
-Neurological problems, cardiac damage
-therefore problem with transketolase
Wernicke-Korsakoff Syndrome
-Genetic defect + thiamine deficiency
-problems with transketolase
-Neurological symptons + Beri Beri-like symptoms
Drug detoxification in liver
-Require NADPH for cytochhrom P-450
Defense against bacteria