HMP pathway Flashcards
HMP pathway occur in ……..
cytoplasm
(in HMP pathway) ……. ATP is directly consumed or produced.
no ATP
(in HMP pathway) oxidation of glucose is direct at …………& produce ……..
carbon 1,3 without cleavage
NADH+H
(in HMP pathway )
glucose6-p is decarboxylated at ……..to produce ……
C1
P-pentose
(in HMP pathway )
oxidative phase is ………but non oxidative phase is ………..
irreversible
reversible
( in HMP pathway )
to enter non-oxidative phase we start with ……………..
3 molecule of ribulose-5P
list fate of products of non-oxidative phase (in HMP pathway)
- if energy is needed :
the glycolytic intermediates “ fructose6-p & glyceraldhyde3-p “continue glycolysis to produce energy. - if there is enough energy :
the glycolytic intermediates regenerate glucose by gluconeogenesis
NADPH-dependent FA synthesis in ………
liver, lactating mammary glands & adipose tissue
NADPH- dependent steroids synthesis in ……
testes , ovaries , placenta & adrenal cortex
NADPH-dependent glutathione reductase in ……………….
erythrocytes
in HMP pathway , the rate limiting enzyme is ………..
G6PD
illustrate the regulation of HMP pathway
- availability of NAD :
accumulation of NADPH allosterically inhibits G6PD. - insulin:
induce G6PD in well fed state
* at level of non-oxidative :
- cell need both NADPH+H & P-pentose = perform oxidative phase only
- cell need NADH+H > P-pentose as in RBCs & fatty acids synthesis in adipose tissue = perform both oxidative & non-oxidative phase to give glycolytic intermediates
- cell need P-pentose > NADPH+H = perform the reverse of non-oxidative phase as in muscle which lack G6PD enzyme
list the importance of HMP pathway
- synthesis of P-pentose
- synthesis of reduced coenzyme NADH+H
list chc of P-pentose synthesis
- no pentokinase in our cells
- P-pentose enter in synthesis of nucleotides
- important in rapidly dividing tissues as BM
- DNA, RNA , ATP , NAD , NADP &cAMP
what’s the importance of NADH+H ?
- used in synthetic reductive pathway as :
FA synthesis , cholesterol , vit D3 & sex H - essential for integrity of RBCs membrane:
- detoxicate H2O2 in RBCs = dec hemolysis
- NADPH+H is important to keep ferrous iron of Hb in its reduced form to prevent accumulation of met Hb - eye lens : maximum con. in lens preserves its transparency
- bactericidal effect :
MQ produce superoxide radical during killing the bacteria , “ respiratory burst “ - synthesis of NO
- endothelium derived relaxing factor (VD)
- prevent platelet aggregation & neurotransmitter - essential for hydroxylation reaction in liver by enzyme cytochrome P450 heme-monooxygenase for detoxification of toxins
list cause of defective transketolase
- deficiency of thiamine pyrophosphate
- defective binding between transketolase & Tpp ( thiamine pyrophosphate)
what’s the clinical picture of defective transketolase?
- neuropsychiatric disorder “ Wernicke Korsakoff syndrome”:
paralysis of eye movement
ataxia “abnormal gait “
defective mental ability
list cause of G6PD deficiency (favism)
- X-linked , affect mainly males
- deficiency of G6PD = dec NADH+H :
- inability to detoxicate H2O2 in RBCs lead to oxidation of membrane proteins , hemolysis
- maintain the reduced state of Hb-SH group
list clinical picture of favism.
- Heinz body :
oxidation of Hb-HS group form denaturated insoluble mass attach to cell membrane - oxidation of membrane proteins make RBCs to be rigid (less deformable) & removed by spleen, liver
- dec Hb level , hemolytic anemia, jaundice and black urine
what’s the precipitating factor ofG6PD deficiency symptoms ?
- fava beans
- antipyretic, antibiotic as sulfa & anti malarial drugs.
- infection “ free radical formed in WBCs can diffuse to RBCs “
list ttt of favism
- avoid this food & drug
- transfusion of packed RBCs
- intake of antioxidant as vit C , E , A