MB+B metabolism Flashcards
how is glycolysis stopped when there are high concentrations of ATP are produced
enzymes are released that prevent the formation of fructose-1,6-biphosphate formation allowing for glucose storage
in liver and muscle cells phosphorylase enzymes can be activated using phosphorylase kinase to make them more reactive
how do fructose and galactose enter glycolysis
they are phosphorylated to form intermediate steps in the pathway such a fructose- 6 phosphate
how is glucose formed from glycogen
the enzyme glycogen phosphorylase hydrolyses the gycosidic bond between a chain of glycogen and phosphorylates one of the residues
how is glucose produced through gluconeogenesis
pyruvate is carboxylated using pyruvate carboxylase into oxyaloacetate. this reacts with guanosine to produce phosphoenolpyruvate. ATP reliant reactions are replaced by phosphatase reactions The phosphoryl groups areremoved by hydrolysis
what does metabolism comprise of
anabolism - rections that require energy
catabolism - reactions that release energy
why does ATP have such high phosphoryl potential
resonance stabilisation
hydration and electrostatic repulsion
what are the steps of gylcolysis
phosphorylation of glucose to make glucose -6- phosphate using hexokinase
conversion to fructose-6-phosphate using phosphoglucose isomerase
further phosphorylation using phosphofructokinase to form fructose-1,6-biphosphate
formation of 2 triose sugars by aldolase to form DHAP and GAP
DHAP is converted to GAP using triose phosphospate isomerase
oxidation of GAP with NAD+ using glyceraldehyde 3 phosphate dehydrogenase to form 1,3-bisphosphateglycerate
ATP production using phosphoglycerate kinase to form 3-phosphate glycerate and ATP
mutated using phosphoglycerate mutase to form 2-phosphate glycerate
dehydration using enolase to form phosphenol pyruvate
pyruvate kinase create an ATP and forms pyruvate
what can form Acetyl CoA
pyruvate, fatty acids and amino acids
what is required to convert pyruvate into Acetyl CoA
pyruvate dehydrogenase
NAD+
FAD
lipoate
TTP
how is pyruvate converted to acetyl coA
release of CO2 triggered by pyruvate dehydrogenase
transfer of acetyl group to CoA through the reduction of lipoate
Oxidation of NAD+ to regenerate lipoate
each cylce of the citric cycle generates what
3 NADH
1 FADH2
2CO2
1 GTP
steps of the citric cycle
the formation of a more reactive carbon for oxidation: citrate through citryl CoA intermediate using citrate synthase
2-5 oxidations
isocitrate using aconitase
alpha ketoglutarate using isocitrate dehydrogenase and forming NADH + CO2
succinyl CoA using alpha ketoglutarate dehydrogenase complex and forming NADH + CO2
succinate using succinyl CoA synthetase anf forming GTP (ATP)
fumarate formed using succinate dehydrogenase create FADH2
hydrate in the presence of fumarase to form malate
oxidised to form oxaloacetate to complete the cycle using malate dehydrogenase and forming NADH
how is the citric acid cycle regulated
pyruvate dehydrogenase, citrate synthese, isocytrate dehydrogenase and alpha- ketoglutarate dehydrogenase are are inhibited by products of the pritate cycle preventing further formation of products
what is the pentose phosphate pathway most typically used in
rapidly dividing cells
what does the pentose phosphate pathway create
pentoses and NADPH
what is the pentose phosphate pathway
glucose-6-phosphate to 6-phosphogluconate forming NADPH from NADP+ and 2GSH from GSSG
ribulose-5-phosphate through the release of CO2 and the formation of NADPH (transkelolase can be used to regenerate this to glucose-6-phosphate)
ribose-5-phosphate
in what context would the regeneration of ribulose-5-phosphate to glucose-6-phosphate be necessary
if needed for glycolysis
or in cells that dont require pentoses
how else can ribose-5-phosphate be aquired when NADPH isnt needed by a cell
fructose-6-phosphate and GAP can be converted in a reverse of the pentose phosphate pathway
what are the types of carriers in the electron transport chain
ubiquinone, cytochrome and iron sulfur centres
what happens in complex 1 of the ETC
NADH donates 2 electrons through Fe-S centres to reduce ubiquinone to ubiquinol allowing it to diffuse into the membrane
4H+ ions are pumped out of the mitochondria into the intermembrane space
what happens in complex 2 of the ETC
succinate is oxidised allowing another molecule of ubiquinone to be reduced and FADH2 donates 2 e- becoming FAD- once again
what happens in complex 3 of the ETC
the ubiquinol formedin complexes 1 + 2 are passed into the complex and the e- and protons pass to cytochrome C. this is soluble and moves throiugh intermembrane space to complex 4
4 protons are pumped into the intermembrane space
what happens in complex 4
4 molecules of cytochrome C bind to the complex and donate and electron each to O2 to produce H2O
2 H+ pumped into the intermembrane space for every 2e- donated to O2
this formsa proton gradient in the intermembrane space
what does the difference in concentration of protons and electrical potential energy cause
proton motive force
how is ATP formed in ETC
the proton motive force cause protons to defuse back through to the matrix through ATP synthase forming ATP
how does poison inhibit the ETC
rotenone inhibits complex 1
antimycin a blocks the process of complex 3
complex 4 blocked by cyanide, azide and CO
alternative uses of mitochondria
newborn mammels have brown adipose tissue that contains lots of mitochondria whose job is to produce heat
how many ATP do NADH andFADH create in the ETC
NADH = 2.5
FADH2 = 1.5
